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1
benign renal tumor 2005:2010[pubdate] *count=100
61504 results
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Items 1 to 100 of about 61504
1.
Oguzkurt P, Ince E, Temiz A, Demir S, Akabolat F, Hicsonmez A:
Prenatal diagnosis of a mass in the adrenal region that proved to be a teratoma.
J Pediatr Hematol Oncol
; 2009 May;31(5):350-1
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[Title]
Prenatal
diagnosis of
a mass in the adrenal region that proved to be a teratoma.
Magnetic resonance imaging showed a 57 x 50 mm mass in the left adrenal region displacing
the kidney
inferiorly.
The infant underwent an adrenalectomy with total resection of the
tumor
, which proved on histologic examination to be a mature teratoma.
Prenatally detected suprarenal masses are likely to be neuroblastoma or adrenal hemorrhage, but may be rare
benign
lesions such as extralobar pulmonary sequestration, bronchogenic cyst, or
renal
dysplasia.
Although teratoma in the adrenal region is extremely rare, it should be included in the clinical and radiologic differential
diagnosis of
prenatally detected suprarenal masses.
Total excision of the mass for histologic
diagnosis
is indicated.
[MeSH-major]
Adrenal Gland
Neoplasms
/ congenital. Adrenal Gland
Neoplasms
/
diagnosis
. Teratoma / congenital. Teratoma /
diagnosis
. Ultrasonography, Prenatal
[MeSH-minor]
Adrenalectomy. Biopsy.
Diagnosis
, Differential. Female. Humans. Infant. Magnetic Resonance Imaging. Male. Pregnancy
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(PMID = 19415017.001).
[ISSN]
1536-3678
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
2.
Verrey F, Singer D, Ramadan T, Vuille-dit-Bille RN, Mariotta L, Camargo SM:
Kidney amino acid transport.
Pflugers Arch
; 2009 May;458(1):53-60
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[Title]
Kidney
amino acid transport.
Near complete reabsorption of filtered amino acids is a main specialized transport function of the
kidney
proximal tubule.
A number of other amino acid transporters expressed in the basolateral membrane of proximal
kidney
tubule cells subserve either specialized metabolic functions, such as the production of ammonium, or are part of the cellular housekeeping equipment.
Some mutations
of B
(0)AT1 differentially interact with these accessory subunits, providing an explanation for differential intestinal phenotypes among Hartnup patients.
The basolateral efflux of numerous amino acids from
kidney
tubular cells is mediated by heteromeric amino acid transporters that function as obligatory exchangers.
[MeSH-major]
Amino Acid Transport Systems / metabolism. Amino Acids / metabolism.
Kidney
/ metabolism
[MeSH-minor]
Amino Acid Transport Systems, Neutral / metabolism. Amino Acid Transport Systems, Neutral / physiology. Animals. Anion Transport Proteins / physiology. Antiporters / physiology. Biological Transport. Humans.
Kidney
Tubules, Proximal / physiology
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[Cites]
Nat Genet. 1999 Mar;21(3):293-6
[
10080182.001
]
[Cites]
Nature. 1996 Oct 17;383(6601):634-7
[
8857541.001
]
[Cites]
J Pharmacol Exp Ther. 2004 Aug;310(2):695-702
[
15051798.001
]
[Cites]
Pflugers Arch. 2005 Nov;451(2):338-48
[
16133263.001
]
[Cites]
Curr Opin Clin Nutr Metab Care. 2000 Jan;3(1):51-7
[
10642084.001
]
[Cites]
Gene. 2002 Jun 12;292(1-2):81-90
[
12119102.001
]
[Cites]
J Biol Chem. 1999 Dec 3;274(49):34948-54
[
10574970.001
]
[Cites]
Am J Clin Nutr. 2004 Feb;79(2):185-97
[
14749222.001
]
[Cites]
Pflugers Arch. 2003 Feb;445(5):529-33
[
12634921.001
]
[Cites]
Nat Genet. 2004 Sep;36(9):999-1002
[
15286787.001
]
[Cites]
J Am Soc Nephrol. 2003 Apr;14(4):837-47
[
12660317.001
]
[Cites]
Physiol Rev. 1998 Oct;78(4):969-1054
[
9790568.001
]
[Cites]
J Biol Chem. 2002 Jun 7;277(23):21017-26
[
11907033.001
]
[Cites]
Physiol Rev. 2008 Jan;88(1):249-86
[
18195088.001
]
[Cites]
J Clin Invest. 2008 Dec;118(12):3881-92
[
19033659.001
]
[Cites]
Nature. 2006 Dec 21;444(7122):1088-91
[
17167413.001
]
[Cites]
EMBO J. 1999 Jan 4;18(1):49-57
[
9878049.001
]
[Cites]
Biochem J. 2005 Aug 1;389(Pt 3):745-51
[
15804236.001
]
[Cites]
Nature. 2004 Oct 14;431(7010):811-8
[
15483603.001
]
[Cites]
Pflugers Arch. 2004 Feb;447(5):465-8
[
14624363.001
]
[Cites]
J Biol Chem. 1996 Jun 21;271(25):14883-90
[
8662767.001
]
[Cites]
Tohoku J Exp Med. 2006 Jan;208(1):25-31
[
16340170.001
]
[Cites]
Biochem Biophys Res Commun. 2003 May 16;304(4):747-54
[
12727219.001
]
[Cites]
Nature. 1992 Dec 3;360(6403):467-71
[
1280334.001
]
[Cites]
Gastroenterology. 2004 Nov;127(5):1410-22
[
15521011.001
]
[Cites]
Am J Physiol Renal Physiol. 2007 Feb;292(2):F555-66
[
17003226.001
]
[Cites]
Am J Physiol Renal Physiol. 2006 Feb;290(2):F376-83
[
16174864.001
]
[Cites]
J Biol Chem. 1998 Dec 4;273(49):32437-45
[
9829974.001
]
[Cites]
Pflugers Arch. 2004 Feb;447(5):610-8
[
12905028.001
]
[Cites]
J Biol Chem. 2004 Jun 4;279(23):24467-76
[
15044460.001
]
[Cites]
J Inherit Metab Dis. 2007 Oct;30(5):716-21
[
17588131.001
]
[Cites]
Am J Physiol. 1997 Dec;273(6 Pt 2):F1023-9
[
9435692.001
]
[Cites]
Am J Physiol Renal Physiol. 2007 Feb;292(2):F533-44
[
16985211.001
]
[Cites]
Annu Rev Nutr. 1995;15:133-59
[
8527215.001
]
[Cites]
FASEB J. 2008 Aug;22(8):2880-7
[
18424768.001
]
[Cites]
Pflugers Arch. 2004 Feb;447(5):776-9
[
12748860.001
]
[Cites]
Am J Physiol Endocrinol Metab. 2002 Feb;282(2):E428-34
[
11788376.001
]
[Cites]
Mol Cell Biol. 2004 May;24(10 ):4166-73
[
15121838.001
]
[Cites]
Biochem J. 2005 Mar 15;386(Pt 3):417-22
[
15689184.001
]
[Cites]
Nature. 2005 Sep 8;437(7056):215-23
[
16041361.001
]
[Cites]
J Membr Biol. 2001 Apr 1;180(3):213-20
[
11337893.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7206-11
[
11390972.001
]
[Cites]
J Membr Biol. 1999 Dec 1;172(3):181-92
[
10568788.001
]
[Cites]
Am J Physiol Cell Physiol. 2001 Sep;281(3):C963-71
[
11502573.001
]
[Cites]
Am J Physiol Renal Physiol. 2001 Jan;280(1):F10-8
[
11133510.001
]
[Cites]
J Membr Biol. 1982;66(3):213-25
[
6808139.001
]
[Cites]
J Biol Chem. 2005 Mar 11;280(10):8974-84
[
15632147.001
]
[Cites]
Gastroenterology. 2009 Mar;136(3):872-82
[
19185582.001
]
[Cites]
Pflugers Arch. 2007 Jun;454(3):507-16
[
17273864.001
]
[Cites]
Curr Probl Clin Biochem. 1976;6:173-89
[
11964.001
]
[Cites]
Physiology (Bethesda). 2006 Apr;21:93-102
[
16565475.001
]
[Cites]
J Cell Physiol. 2006 Mar;206(3):771-9
[
16245314.001
]
[Cites]
Annu Rev Physiol. 2005;67:557-72
[
15709970.001
]
[Cites]
Physiol Rev. 1990 Jan;70(1):43-77
[
2404290.001
]
[Cites]
J Biol Chem. 2003 Jan 10;278(2):1316-22
[
12417581.001
]
[Cites]
Nat Genet. 1999 Mar;21(3):297-301
[
10080183.001
]
[Cites]
J Am Soc Nephrol. 2005 Apr;16(4):869-77
[
15716335.001
]
[Cites]
Am J Physiol Renal Physiol. 2003 May;284(5):F885-92
[
12676733.001
]
[Cites]
J Biol Chem. 2006 Sep 8;281(36):26552-61
[
16825196.001
]
[Cites]
Nat Genet. 2004 Sep;36(9):1003-7
[
15286788.001
]
(PMID = 19184091.001).
[ISSN]
1432-2013
[Journal-full-title]
Pflugers Archiv : European journal of physiology
[ISO-abbreviation]
Pflugers Arch.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Amino Acid Transport Systems; 0 / Amino Acid Transport Systems, Neutral; 0 / Amino Acids; 0 / Anion Transport Proteins; 0 / Antiporters; 0 / SLC26A8 protein, human; 0 / SLC6A19 protein, human
[Number-of-references]
60
3.
Zhou Y, Vaidya VS, Brown RP, Zhang J, Rosenzweig BA, Thompson KL, Miller TJ, Bonventre JV, Goering PL:
Comparison of kidney injury molecule-1 and other nephrotoxicity biomarkers in urine and kidney following acute exposure to gentamicin, mercury, and chromium.
Toxicol Sci
; 2008 Jan;101(1):159-70
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[Title]
Comparison
of kidney
injury molecule-1 and other nephrotoxicity biomarkers in urine and
kidney
following acute exposure to gentamicin, mercury, and chromium.
Sensitive biomarkers are needed to detect
kidney
injury at the earliest stages.
The objective of this study was to determine whether the appearance
of kidney
injury molecule-1 (Kim-1) protein ectodomain in urine and
kidney
injury molecule-1/hepatitis A viral cellular receptor-1 (Kim-1/Havcr1) gene expression in
kidney
tissue may be more predictive of
renal
injury after exposure to nephrotoxicants when compared to traditionally used biomarkers.
The results showed that increases in urinary Kim-1 and
kidney
Kim-1/Havcr1 gene expression paralleled the degree of severity of
renal
histopathology and were detected at lower doses of nephrotoxicants when compared to blood urea nitrogen (BUN), serum creatinine, and urinary N-acetyl-beta-D-glucosaminidase (NAG).
Urinary Kim-1 and
kidney
Kim-1/Havcr1 expression appear to be sensitive and tissue-specific biomarkers that will improve detection of early acute
kidney
injury following exposure to nephrotoxic chemicals and drugs.
MedlinePlus Health Information.
consumer health - Kidney Diseases
.
MedlinePlus Health Information.
consumer health - Mercury
.
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MERCURY, ELEMENTAL
.
Hazardous Substances Data Bank.
CHROMIUM, ELEMENTAL
.
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[Cites]
Acta Vitaminol Enzymol. 1984;6(2):103-7
[
6496253.001
]
[Cites]
Am J Physiol Renal Physiol. 2007 Jan;292(1):F313-20
[
16896183.001
]
[Cites]
Environ Health Perspect. 1991 May;92:71-4
[
1935854.001
]
[Cites]
Pharmacol Toxicol. 1991 May;68(5):317-21
[
1946176.001
]
[Cites]
Gen Pharmacol. 1995 Nov;26(7):1477-87
[
8690234.001
]
[Cites]
EMBO J. 1996 Aug 15;15(16):4282-96
[
8861957.001
]
[Cites]
Drug Saf. 1997 Mar;16(3):205-31
[
9098657.001
]
[Cites]
J Biol Chem. 1998 Feb 13;273(7):4135-42
[
9461608.001
]
[Cites]
Toxicol Pathol. 1998 Jan-Feb;26(1):92-103
[
9502391.001
]
[Cites]
J Virol. 1998 Aug;72(8):6621-8
[
9658108.001
]
[Cites]
J Am Soc Nephrol. 2005 Apr;16(4):1126-34
[
15744000.001
]
[Cites]
BMC Nephrol. 2005;6:4
[
15854231.001
]
[Cites]
J Am Soc Nephrol. 2005 Nov;16(11):3365-70
[
16177006.001
]
[Cites]
Am J Physiol Renal Physiol. 2006 Feb;290(2):F517-29
[
16174863.001
]
[Cites]
J Am Soc Nephrol. 2007 Mar;18(3):904-12
[
17267747.001
]
[Cites]
Am J Surg Pathol. 2007 Mar;31(3):371-81
[
17325478.001
]
[Cites]
Ren Fail. 2002 Nov;24(6):687-90
[
12472192.001
]
[Cites]
Free Radic Biol Med. 2003 Jun 1;34(11):1390-8
[
12757849.001
]
[Cites]
Toxicol Sci. 2003 Sep;75(1):208-22
[
12832660.001
]
[Cites]
Am J Physiol Renal Physiol. 2004 Mar;286(3):F552-63
[
14600030.001
]
[Cites]
Am J Med. 1968 May;44(5):664-705
[
5646427.001
]
[Cites]
Toxicol Appl Pharmacol. 1980 Jul;54(3):443-53
[
6446781.001
]
[Cites]
J Toxicol Environ Health. 1982 Jan;9(1):119-26
[
6460873.001
]
[Cites]
Biochem Pharmacol. 1982 Oct 1;31(19):3093-100
[
6216890.001
]
[Cites]
Pharmacol Rev. 2000 Mar;52(1):113-43
[
10699157.001
]
[Cites]
Therapie. 2000 Jan-Feb;55(1):91-6
[
10860006.001
]
[Cites]
J Environ Sci Health B. 2001 Sep;36(5):687-97
[
11599730.001
]
[Cites]
Kidney Int. 2002 Jul;62(1):237-44
[
12081583.001
]
[Cites]
Cleve Clin J Med. 2002 Jul;69(7):569-74
[
12109642.001
]
[Cites]
J Biol Chem. 2002 Oct 18;277(42):39739-48
[
12138159.001
]
[Cites]
Kidney Int. 1991 Apr;39(4):639-46
[
1711136.001
]
[Cites]
Am J Physiol Renal Physiol. 2006 Aug;291(2):F456-64
[
16467126.001
]
[Cites]
Am J Physiol Renal Physiol. 2007 Jan;292(1):F131-9
[
16835406.001
]
[Cites]
Am J Physiol Renal Physiol. 2002 Dec;283(6):F1326-36
[
12388382.001
]
(PMID = 17934191.001).
[ISSN]
1096-6080
[Journal-full-title]
Toxicological sciences : an official journal of the Society of Toxicology
[ISO-abbreviation]
Toxicol. Sci.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK 072831; United States / NIEHS NIH HHS / ES / ES016723-02; United States / NIDDK NIH HHS / DK / R37 DK039773; United States / NIDDK NIH HHS / DK / DK 074099; United States / NIDDK NIH HHS / DK / R01 DK072381-04; United States / NIDDK NIH HHS / DK / R01 DK072381; United States / NIDDK NIH HHS / DK / R33 DK074099; United States / NIEHS NIH HHS / ES / R00 ES016723-02; United States / NIDDK NIH HHS / DK / DK 039773; United States / NIDDK NIH HHS / DK / R21 DK074099; United States / NIEHS NIH HHS / ES / R00 ES016723; United States / NIDDK NIH HHS / DK / R01 DK039773; None / None / / R01 DK072381-04
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers; 0 / Cell Adhesion Molecules; 0 / Gentamicins; 0 / Havcr1protein, rat; 0 / Membrane Proteins; 0 / Protein Synthesis Inhibitors; 0R0008Q3JB / Chromium; 63231-63-0 / RNA; 7535-00-4 / Galactosamine; FXS1BY2PGL / Mercury; V956696549 / Acetylglucosamine
[Other-IDs]
NLM/ NIHMS110357; NLM/ PMC2744478
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4.
Petillo D, Kort EJ, Anema J, Furge KA, Yang XJ, Teh BT:
MicroRNA profiling of human kidney cancer subtypes.
Int J Oncol
; 2009 Jul;35(1):109-14
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[Title]
MicroRNA profiling of human
kidney
cancer subtypes.
In order to understand their role in
renal
tumorigenesis, we screened the expression levels of miRNAs in four subtypes of human
renal
neoplasms
: clear cell, papillary, and chromophobe
renal
cell carcinomas (RCC) as well as
benign renal
oncocytomas.
We found a unique miRNA signature for each subtype of
renal tumor
.
Specifically, we documented the overexpression of miRs 424 and 203 in clear cell RCC relative to papillary RCC, as well as the inversion of expression of miR-203 in the
benign
oncocytomas (where it is underexpressed relative to normal
kidney
) as compared to the malignant chromophobe RCC (where it is overexpressed relative to normal
kidney
).
While previous studies have identified unique miRNA expression pattern distinguishing
tumors
from different anatomical locations, here we extend this principle to demonstrate the utility of miRNA expression profiling to identify a signature unique to various
tumor
subtypes at a single anatomic locus.
[MeSH-major]
Adenoma, Oxyphilic / genetics. Carcinoma,
Renal
Cell / genetics. Gene Expression Profiling / methods.
Kidney Neoplasms
/ genetics. MicroRNAs / analysis
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(PMID = 19513557.001).
[ISSN]
1019-6439
[Journal-full-title]
International journal of oncology
[ISO-abbreviation]
Int. J. Oncol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / MicroRNAs
5.
Boorjian SA, Frank I, Inman B, Lohse CM, Cheville JC, Leibovich BC, Blute ML:
The role of partial nephrectomy for the management of sporadic renal angiomyolipoma.
Urology
; 2007 Dec;70(6):1064-8
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[Title]
The role of partial nephrectomy for the management of sporadic
renal
angiomyolipoma.
OBJECTIVES: Angiomyolipoma is a
benign renal tumor
that has a propensity to grow over time and may cause local complications.
Given the
benign
nature of these lesions,
renal
-preserving treatments are favored.
We evaluated our experience with nephron-sparing surgery for
renal
angiomyolipoma.
METHODS: We reviewed our institutional nephrectomy registry to identify patients treated with nephron-sparing surgery for
renal
angiomyolipoma between 1970 and 2004.
Patients with a
diagnosis of
tuberous sclerosis were excluded.
RESULTS: We identified 58 patients treated with nephron-sparing surgery for sporadic
renal
angiomyolipoma, including 44 women and 14 men.
The median
tumor
size was 3.9 cm (range, 0.8-12.5 cm).
No patient developed de novo chronic
renal
insufficiency after nephron-sparing surgery, including 4 patients treated for angiomyolipomas in a solitary
kidney
.
CONCLUSIONS: Nephron-sparing surgery for sporadic
renal
angiomyolipomas offers preservation of
renal
function and is associated with acceptable complication and low local recurrence rates.
[MeSH-major]
Angiomyolipoma / surgery.
Kidney Neoplasms
/ surgery. Nephrectomy
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(PMID = 18158015.001).
[ISSN]
1527-9995
[Journal-full-title]
Urology
[ISO-abbreviation]
Urology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
6.
Resende L, Guerra J, Santana A, Mil-Homens C, Abreu F, da Costa AG:
Influence of dialysis duration and modality on kidney transplant outcomes.
Transplant Proc
; 2009 Apr;41(3):837-9
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[Title]
Influence of dialysis duration and modality on
kidney
transplant outcomes.
BACKGROUND: The influence of pretransplantation dialysis on
kidney
transplant outcomes has been the subject of longstanding interest.
Although increased time on dialysis prior to
kidney
transplantation is associated with decreased graft and patient survivals, analyses of the impact of dialysis modality on
kidney
allograft outcome have produced conflicting results.
OBJECTIVE: The objective of this study was to evaluate the influence of dialysis duration and modality on the function and survival of
renal
allografts.
PATIENTS: We retrospectively reviewed the clinical data of 421 adults who received first
kidney
transplantations from cadaveric heart-beating donors performed in our unit from May 1989 to May 2007.
Three hundred seventy-four patients (88.8%) were on hemodialysis (HD) prior to
kidney
transplantation, including 247 patients (58.7%) on treatment for at least 24 months.
Renal
function at 3, 12, 60, and 96 months was similar between the 2 groups.
No differences were observed in
renal
function or graft and patient survivals comparing HD or peritoneal dialysis (PD).
[MeSH-major]
Kidney
Failure, Chronic / surgery.
Kidney
Transplantation / physiology.
Renal
Dialysis
[MeSH-minor]
Adult. Age Factors. Female. Graft Survival. Humans.
Kidney
Function Tests. Living Donors. Male. Middle Aged. Postoperative Complications / epidemiology. Retrospective Studies. Sex Characteristics. Survival Analysis. Survivors. Time Factors. Tissue Donors / supply & distribution. Treatment Outcome. Young Adult
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(PMID = 19376365.001).
[ISSN]
0041-1345
[Journal-full-title]
Transplantation proceedings
[ISO-abbreviation]
Transplant. Proc.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
7.
Casas-Aparicio G, Castillo-Martínez L, Orea-Tejeda A, Abasta-Jiménez M, Keirns-Davies C, Rebollar-González V:
The effect of successful kidney transplantation on ventricular dysfunction and pulmonary hypertension.
Transplant Proc
; 2010 Nov;42(9):3524-8
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[Title]
The effect of successful
kidney
transplantation on ventricular dysfunction and pulmonary hypertension.
BACKGROUND: Heart disease is a frequent complication of chronic
kidney
disease and the major cause of death in patients on
renal
replacement therapy.
The purpose of this study was to evaluate the impact of successful
kidney
transplantation on systolic and diastolic ventricular dysfunction and pulmonary arterial hypertension in patients with chronic
kidney
disease (CKD).
METHODS: The study included 35 patients >18 years of age with CKD who had successful
kidney
transplantations.
The LVEF of the entire group increased from 52% to 64% (P < .001) by 12 months after
kidney
transplant.
CONCLUSIONS: Because
kidney
transplantation led to considerable improvement in left ventricular systolic and diastolic function as well as pulmonary arterial pressure of patients with CKD, optimal treatment for dysfunction and transplant as soon as possible is recommended.
[MeSH-major]
Hypertension, Pulmonary / etiology.
Kidney
Failure, Chronic / surgery.
Kidney
Transplantation. Ventricular Dysfunction, Left / etiology
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[Copyright]
Copyright © 2010 Elsevier Inc. All rights reserved.
(PMID = 21094809.001).
[ISSN]
1873-2623
[Journal-full-title]
Transplantation proceedings
[ISO-abbreviation]
Transplant. Proc.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
8.
Canales MT, Kasiske BL, Rosenberg ME:
Transplant tourism: Outcomes of United States residents who undergo kidney transplantation overseas.
Transplantation
; 2006 Dec 27;82(12):1658-61
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[Title]
Transplant tourism: Outcomes of United States residents who undergo
kidney
transplantation overseas.
BACKGROUND: Although international commerce in
kidney
transplantation is a reality, little is known about U.S. residents who travel abroad for
kidney
transplantation.
METHODS: We retrospectively reviewed the clinical outcomes of patients who were evaluated at the University of Minnesota Medical Center or Hennepin County Medical Center, but then surreptitiously underwent
kidney
transplantation overseas.
RESULTS: We identified 10 patients who underwent
kidney
transplantation outside the United States between September 16, 2002 and June 30, 2006 and then returned for care in our programs.
CONCLUSIONS:
Kidney
function and graft survival were generally good after surreptitious overseas
kidney
transplantation.
[MeSH-major]
Graft Survival.
Kidney
Transplantation. Travel
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(PMID = 17198255.001).
[ISSN]
0041-1337
[Journal-full-title]
Transplantation
[ISO-abbreviation]
Transplantation
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
9.
Mosconi G, Panicali L, Persici E, Conte D, Cappuccilli ML, Cuna V, Capelli I, Todeschini P, D'Arcangelo GL, Stefoni S:
Native kidney function after renal transplantation combined with other solid organs in preemptive patients.
Transplant Proc
; 2010 May;42(4):1017-20
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[Title]
Native
kidney
function after
renal
transplantation combined with other solid organs in preemptive patients.
Kidney
transplantations combined with other solid organs are progressively increasing in number.
There are no guidelines regarding the nephrologic indications for combined transplantations, namely liver-
kidney
(LKT), or heart-
kidney
(HKT), in preemptive patients with chronic
kidney
failure who are not on regular dialysis therapy.
The objective of this study was to assess the functional contribution of the native
kidneys
after preemptive
kidney
transplantation combined with other solid organs.
From 2004, 9 patients (aged 50.3 +/- 8.5 years) with chronic
kidney
failure (creatinine 2.5 +/- 1.0 mg/dL) caused by polycystic
kidney
disease (n = 4), vascular nephropathy (n = 2), interstitial nephropathy (n = 1), glomerulonephritis (n = 1), or end-stage
kidney
disease (n = 1), underwent combined transplantations (8 LKT, 1 HKT).
A scintigraphic functional study (Tc-99DMSA or Tc-99mMAG3), was performed at 4 +/- 3 months after transplantation to evaluate the functional contribution of both the native
kidneys
and the graft.
At the time of scintigraphy,
renal
function in all patients was 1.3 +/- 0.3 mg/dL.
The functional contribution of the transplanted
kidneys
was on average 77 +/- 18%.
At follow-up after 36 months, patient and
kidney
survivals were 100%.
The study confirmed a high risk of loss of native
kidney
function in the presence of organic nephropathy.
[MeSH-major]
Kidney
Transplantation / physiology. Organ Transplantation / physiology
[MeSH-minor]
Adult. Creatinine / blood. Female. Glomerular Filtration Rate. Heart Transplantation / physiology. Humans.
Kidney
Diseases / classification.
Kidney
Diseases / surgery.
Kidney
Failure, Chronic / surgery.
Kidney
Function Tests. Liver Transplantation / physiology. Male. Middle Aged. Polycystic
Kidney
Diseases / surgery
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[Copyright]
Copyright (c) 2010. Published by Elsevier Inc.
(PMID = 20534213.001).
[ISSN]
1873-2623
[Journal-full-title]
Transplantation proceedings
[ISO-abbreviation]
Transplant. Proc.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
AYI8EX34EU / Creatinine
10.
Sundaram S, Tasker AD, Morrell NW:
Familial spontaneous pneumothorax and lung cysts due to a Folliculin exon 10 mutation.
Eur Respir J
; 2009 Jun;33(6):1510-2
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In 1977, Birt, Hogg and Dube (BHD) described a genodermatosis characterised by
benign
tumours of the hair follicle that has been associated with
renal
neoplasms
and spontaneous pneumothorax.
In addition, we report an antenatal
diagnosis
(34 weeks gestation) of lung cysts in one affected family member.
Genetic analysis in the family has revealed a unique deletion mutation (c. 1537
del
-C) involving exon 10.
[MeSH-major]
Cysts / genetics. Lung Diseases / genetics. Pneumothorax / genetics. Proto-Oncogene Proteins / genetics.
Tumor
Suppressor Proteins / genetics
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(PMID = 19483054.001).
[ISSN]
1399-3003
[Journal-full-title]
The European respiratory journal
[ISO-abbreviation]
Eur. Respir. J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Contrast Media; 0 / FLCN protein, human; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins
11.
Jiang JC, Li CG, Liang QQ, Bian Q, Zhou Q, Cui XJ, Huang M, Liu QG, Lu S, Zhou CJ, Shi Q, Wang YJ:
[Establishment of a rat model of cervical syndrome with kidney deficiency].
Zhong Xi Yi Jie He Xue Bao
; 2008 Oct;6(10):1034-9
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[Title]
[Establishment of a rat model of cervical syndrome with
kidney
deficiency].
OBJECTIVE: To establish a rat model of cervical syndrome (CS) with
kidney
deficiency.
METHODS: A group of 30 three-month-old female Sprague-Dawley rats were randomly divided into normal control group, CS group and CS with
kidney
deficiency group (combined group), with 10 rats in each group.
Rats in the normal control group received no treatment, rats in the CS group underwent only resection of cervical muscles and ligaments as unbalanced dynamic and static animal model, and rats in combined group underwent resection of both cervical muscles and ovaries as
kidney
deficiency model.
Kidney
deficiency was determined by observing the morphologic changes of uterus and appendages, detecting the weight of uterus and appendages and the content of serum estradiol (E(2)).
CONCLUSION: The rat model of CS with
kidney
deficiency is established.
Kidney
deficiency can aggravate cervical intervertebral disc degeneration.
[MeSH-minor]
Animals. Female.
Kidney
Diseases. Ovariectomy. Random Allocation. Rats. Rats, Sprague-Dawley
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(PMID = 18847538.001).
[ISSN]
1672-1977
[Journal-full-title]
Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine
[ISO-abbreviation]
Zhong Xi Yi Jie He Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
12.
El-Agroudy AE, Sabry AA, Wafa EW, Neamatalla AH, Ismail AM, Mohsen T, Khalil AA, Shokeir AA, Ghoneim MA:
Long-term follow-up of living kidney donors: a longitudinal study.
BJU Int
; 2007 Dec;100(6):1351-5
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[Title]
Long-term follow-up of living
kidney
donors: a longitudinal study.
OBJECTIVE: To analyse retrospectively the general health status and
renal
and cardiovascular consequences of living-related
kidney
donation, as the long-term effects of unilateral nephrectomy for
kidney
donation are of particular interest with the currently increasing practice of living-donor transplantation.
PATIENTS AND METHODS: Living-related
kidney
donors (1400) who had donated their
kidneys
between 1976 and 2002 were asked to attend a dedicated donor follow-up clinic starting in 2004.
We attempted to contact all donors to determine the long-term outcome of their remaining
kidney
.
All
kidney
donors who responded had a detailed assessment, and were questioned about rehabilitation and their feelings on donating a
kidney
.
[MeSH-major]
Health Status.
Kidney
. Living Donors. Nephrectomy / adverse effects. Tissue and Organ Harvesting / adverse effects
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(PMID = 17941927.001).
[ISSN]
1464-410X
[Journal-full-title]
BJU international
[ISO-abbreviation]
BJU Int.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
13.
Kestenbaum B, Rudser KD, de Boer IH, Peralta CA, Fried LF, Shlipak MG, Palmas W, Stehman-Breen C, Siscovick DS:
Differences in kidney function and incident hypertension: the multi-ethnic study of atherosclerosis.
Ann Intern Med
; 2008 Apr 1;148(7):501-8
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[Title]
Differences in
kidney
function and incident hypertension: the multi-ethnic study of atherosclerosis.
BACKGROUND:
Kidney
disease and hypertension commonly coexist, yet the direction of their association is still debated.
OBJECTIVE: To evaluate whether early
kidney
dysfunction, measured by serum cystatin C levels and urinary albumin excretion, predates hypertension in adults without clinically recognized
kidney
or cardiovascular disease.
PARTICIPANTS: 2767 MESA participants without prevalent hypertension, cardiovascular disease, or clinically recognized
kidney
disease (an estimated glomerular filtration rate <60 mL/min per 1.73 m2 or microalbuminuria).
LIMITATIONS: Unmeasured characteristics may have confounded observed associations
of kidney
markers with hypertension.
CONCLUSION: Differences in
kidney
function, indicated by cystatin C levels, are associated with incident hypertension among individuals without clinical
kidney
or cardiovascular disease.
These population-based findings complement experimental work implicating early
kidney
damage in the pathogenesis of essential hypertension.
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[Cites]
Am J Kidney Dis. 1996 Dec;28(6):811-21
[
8957032.001
]
[Cites]
J Hum Hypertens. 1996 Oct;10(10):691-4
[
9004096.001
]
[Cites]
Diabetes Care. 1998 Jul;21(7):1076-9
[
9653598.001
]
[Cites]
Ann Intern Med. 1999 Mar 16;130(6):461-70
[
10075613.001
]
[Cites]
Scand J Clin Lab Invest. 1999 Feb;59(1):1-8
[
10206092.001
]
[Cites]
Lancet. 1963 Mar 30;1(7283):677-82
[
14014100.001
]
[Cites]
Circulation. 2005 Mar 22;111(11):1370-6
[
15738353.001
]
[Cites]
Am J Transplant. 2001 Sep;1(3):222-7
[
12102255.001
]
[Cites]
Lancet. 2002 Aug 31;360(9334):659-65
[
12241871.001
]
[Cites]
Arch Intern Med. 2005 Apr 25;165(8):923-8
[
15851645.001
]
[Cites]
Kidney Int. 2005 Jun;67(6):2089-100
[
15882252.001
]
[Cites]
N Engl J Med. 2005 May 19;352(20):2049-60
[
15901858.001
]
[Cites]
Kidney Int Suppl. 2005 Aug;(97):S68-77
[
16014104.001
]
[Cites]
Mayo Clin Proc. 2005 Oct;80(10):1270-7
[
16212138.001
]
[Cites]
J Am Soc Nephrol. 2006 Feb;17(2):331-5
[
16434504.001
]
[Cites]
Ann Intern Med. 2006 Aug 15;145(4):247-54
[
16908915.001
]
[Cites]
Am J Kidney Dis. 2000 Jul;36(1):29-34
[
10873868.001
]
[Cites]
N Engl J Med. 2002 Mar 21;346(12):913-23
[
11907292.001
]
[Cites]
J Am Soc Nephrol. 2002 Apr;13(4):1034-9
[
11912263.001
]
[Cites]
Am J Epidemiol. 2002 Nov 1;156(9):871-81
[
12397006.001
]
[Cites]
Am J Kidney Dis. 2003 Jan;41(1):1-12
[
12500213.001
]
[Cites]
N Engl J Med. 2003 Jan 9;348(2):101-8
[
12519920.001
]
[Cites]
Diabetes Care. 2003 Nov;26(11):3160-7
[
14578255.001
]
[Cites]
Hypertension. 2003 Dec;42(6):1206-52
[
14656957.001
]
[Cites]
Kidney Int. 2004 Apr;65(4):1416-21
[
15086483.001
]
[Cites]
Am J Med. 1972 May;52(5):584-94
[
4337474.001
]
[Cites]
Circ Res. 1975 Jun;36(6):692-6
[
1093748.001
]
[Cites]
J Clin Invest. 1986 Jun;77(6):1993-2000
[
3011863.001
]
[Cites]
Arch Intern Med. 1987 May;147(5):943-4
[
3555378.001
]
[Cites]
J Clin Epidemiol. 1992 Jun;45(6):683-92
[
1607909.001
]
[Cites]
N Engl J Med. 1992 Jul 16;327(3):151-6
[
1608406.001
]
[Cites]
Lancet. 1992 Dec 12;340(8833):1435-6
[
1360561.001
]
[Cites]
BMJ. 1993 Jan 2;306(6869):24-7
[
8435572.001
]
[Cites]
Hypertension. 1994 Sep;24(3):301-8
[
8082936.001
]
[Cites]
Kidney Int. 1995 Jan;47(1):312-8
[
7731163.001
]
[Cites]
Clin Exp Hypertens. 1996 Apr-May;18(3-4):305-21
[
8743023.001
]
[Cites]
Circulation. 1996 Sep 15;94(6):1310-5
[
8822985.001
]
[CommentIn]
Ann Intern Med. 2008 Aug 19;149(4):284; author reply 284
[
18711167.001
]
(PMID = 18378946.001).
[ISSN]
1539-3704
[Journal-full-title]
Annals of internal medicine
[ISO-abbreviation]
Ann. Intern. Med.
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HC / N01-HC-95162; United States / NHLBI NIH HHS / HC / N01-HC-95163; United States / NHLBI NIH HHS / HL / N01HC95169; United States / NHLBI NIH HHS / HC / N01-HC-95159; United States / NCRR NIH HHS / RR / KL2 RR025015-01; United States / NHLBI NIH HHS / HC / N01-HC-95165; United States / NCATS NIH HHS / TR / TL1 TR000422; United States / NHLBI NIH HHS / HC / N01-HC-95169; United States / NHLBI NIH HHS / HC / N01-HC-95164; United States / NHLBI NIH HHS / HL / N01HC95165; United States / NHLBI NIH HHS / HL / N01HC95159; United States / NHLBI NIH HHS / HC / N01-HC-95160; United States / NIDDK NIH HHS / DK / K23 DK63274-01; United States / NCRR NIH HHS / RR / KL2 RR025015; United States / NHLBI NIH HHS / HC / N01-HC-95161; United States / NCATS NIH HHS / TR / UL1 TR000423; United States / NIDDK NIH HHS / DK / K23 DK063274
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / CST3 protein, human; 0 / Cystatin C; 0 / Cystatins; AYI8EX34EU / Creatinine
[Other-IDs]
NLM/ NIHMS267500; NLM/ PMC3044648
14.
Ranganathan N, Ranganathan P, Friedman EA, Joseph A, Delano B, Goldfarb DS, Tam P, Rao AV, Anteyi E, Musso CG:
Pilot study of probiotic dietary supplementation for promoting healthy kidney function in patients with chronic kidney disease.
Adv Ther
; 2010 Sep;27(9):634-47
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[Title]
Pilot study of probiotic dietary supplementation for promoting healthy
kidney
function in patients with chronic
kidney
disease.
INTRODUCTION: Uremic syndrome consists of nitrogenous waste retention, deficiency in
kidney
-derived hormones, and reduced acid excretion, and, if untreated, may progress to coma and eventual death.
Previous experience suggests that oral administration of a probiotic formulation of selected microbial strains may extend renoprotection via intraintestinal extraction of toxic waste solutes in patients with chronic
kidney
disease (CKD)stages 3 and 4.
[MeSH-major]
Probiotics.
Renal
Insufficiency, Chronic / therapy. Uremia / prevention & control
[MeSH-minor]
Adult. Aged. Argentina. Canada. Creatinine / analysis. Dietary Supplements / standards. Disease Progression. Double-Blind Method. Female. Humans.
Kidney
Function Tests. Male. Middle Aged. Nigeria. Pilot Projects. Protective Agents / pharmacokinetics. Quality of Life. Self Report. Treatment Outcome. United States. Uric Acid / analysis. Young Adult
Genetic Alliance.
consumer health - Kidney Disease
.
MedlinePlus Health Information.
consumer health - Chronic Kidney Disease
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
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(PMID = 20721651.001).
[ISSN]
1865-8652
[Journal-full-title]
Advances in therapy
[ISO-abbreviation]
Adv Ther
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Randomized Controlled Trial
[Publication-country]
United States
[Chemical-registry-number]
0 / Protective Agents; 268B43MJ25 / Uric Acid; AYI8EX34EU / Creatinine
15.
Veroux M, Corona D, Giuffrida G, Gagliano M, Vizcarra D, Tallarita T, Zerbo D, Giaquinta A, Sorbello M, Macarone M, Veroux P:
Sirolimus-based immunosuppression in kidney transplantation for type 2 diabetic nephropathy.
Urol Int
; 2010;84(3):301-4
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[Title]
Sirolimus-based immunosuppression in
kidney
transplantation for type 2 diabetic nephropathy.
INTRODUCTION:
Kidney
transplantation is the best replacement therapy of type 2 diabetic patients and recently similar graft and patient survival between diabetic and nondiabetic recipients has been reported.
We present our experience with sirolimus-based immunosuppression in a population of 24 type 2 diabetic patients who underwent a
kidney
transplantation.
PATIENTS AND METHODS: From January 2001 to December 2006, 396
kidney
transplantations were performed.
Twenty-four patients had type 2 diabetes mellitus as a cause of end-stage
renal
disease.
A slightly better
kidney
functionality was observed in group B patients.
CONCLUSIONS: Sirolimus-based immunosuppression is safe and efficacious in type 2 diabetic patients who underwent a
kidney
transplantation, allowing a better glucose metabolism control.
[MeSH-major]
Diabetes Mellitus, Type 2 / complications. Diabetic Nephropathies / etiology. Diabetic Nephropathies / surgery. Immunosuppression. Immunosuppressive Agents / therapeutic use.
Kidney
Transplantation. Sirolimus / therapeutic use
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Diabetes Type 2
.
MedlinePlus Health Information.
consumer health - Diabetic Kidney Problems
.
MedlinePlus Health Information.
consumer health - Kidney Transplantation
.
Hazardous Substances Data Bank.
SIROLIMUS
.
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[Copyright]
Copyright 2010 S. Karger AG, Basel.
(PMID = 20389159.001).
[ISSN]
1423-0399
[Journal-full-title]
Urologia internationalis
[ISO-abbreviation]
Urol. Int.
[Language]
eng
[Publication-type]
Journal Article; Randomized Controlled Trial
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Immunosuppressive Agents; W36ZG6FT64 / Sirolimus
16.
Yan BC, Gong C, Song J, Krausz T, Tretiakova M, Hyjek E, Al-Ahmadie H, Alves V, Xiao SY, Anders RA, Hart JA:
Arginase-1: a new immunohistochemical marker of hepatocytes and hepatocellular neoplasms.
Am J Surg Pathol
; 2010 Aug;34(8):1147-54
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[Title]
Arginase-1: a new immunohistochemical marker of hepatocytes and hepatocellular
neoplasms
.
The distinction of hepatocellular carcinoma (HCC) from metastatic
tumor
in the liver often presents a diagnostic challenge that carries significant impact on prognostication and therapy.
The sensitivities of Arg-1 in well, moderately, and poorly differentiated HCCs are 100%, 96.2%, and 85.7%, respectively, whereas, in comparison, HepPar-1 demonstrated sensitivities of 100%, 83.0%, and 46.4% for well, moderately, and poorly differentiated
tumors
, respectively.
We also examined Arg-1 expression in nonhepatocellular
tumors
, including many that are potential mimics of HCC (
renal
cell carcinomas, neuroendocrine
tumors
, melanomas, gastric adenocarcinomas, and adrenocortical carcinomas) and found that only 2 non-HCC
tumors
were reactive for Arg-1.
Arg-1 represents a sensitive and specific marker of
benign
and malignant hepatocytes that may ultimately prove to be a useful diagnostic tool in routine surgical pathology practice.
[MeSH-major]
Arginase / analysis. Biomarkers,
Tumor
/ analysis. Carcinoma, Hepatocellular / enzymology. Hepatocytes / enzymology. Immunohistochemistry. Liver
Neoplasms
/ enzymology
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consumer health - Liver Cancer
.
The Lens.
Cited by Patents in
.
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[Cites]
Curr Opin Clin Nutr Metab Care. 1998 Jul;1(4):335-9
[
10565370.001
]
[Cites]
J Biomed Biotechnol. 2010;2010:683485
[
20029630.001
]
[Cites]
Am J Clin Pathol. 2001 May;115(5):689-94
[
11345832.001
]
[Cites]
Am J Surg Pathol. 2002 Aug;26(8):978-88
[
12170084.001
]
[Cites]
Hum Pathol. 2002 Dec;33(12):1175-81
[
12514785.001
]
[Cites]
Mod Pathol. 2003 Feb;16(2):137-44
[
12591966.001
]
[Cites]
Am J Clin Pathol. 2003 Mar;119(3):361-6
[
12645337.001
]
[Cites]
J Immunol. 2004 Jun 15;172(12):7565-73
[
15187136.001
]
[Cites]
Am J Clin Pathol. 2004 Jun;121(6):884-92
[
15198362.001
]
[Cites]
J Cancer Res Clin Oncol. 2004 Sep;130(9):514-20
[
15221469.001
]
[Cites]
J Nutr. 2004 Oct;134(10 Suppl):2820S-2825S; discussion 2853S
[
15465793.001
]
[Cites]
Histochemistry. 1987;87(5):465-70
[
3323144.001
]
[Cites]
Am J Pathol. 1993 Oct;143(4):1050-4
[
7692729.001
]
[Cites]
Int J Dev Neurosci. 1994 Jun;12(4):337-42
[
7976488.001
]
[Cites]
Mod Pathol. 1997 Jul;10(7):686-92
[
9237179.001
]
[Cites]
J Immunol. 1998 Jun 1;160(11):5347-54
[
9605134.001
]
[Cites]
Mod Pathol. 1998 Oct;11(10):934-8
[
9796718.001
]
[Cites]
Histopathology. 1998 Oct;33(4):318-24
[
9822920.001
]
[Cites]
Blood. 2005 Mar 15;105(6):2549-56
[
15546957.001
]
[Cites]
CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108
[
15761078.001
]
[Cites]
Acta Cytol. 2006 May-Jun;50(3):257-62
[
16780018.001
]
[Cites]
Anal Quant Cytol Histol. 2006 Aug;28(4):181-7
[
16927637.001
]
[Cites]
Virchows Arch. 2006 Sep;449(3):308-14
[
16896894.001
]
[Cites]
Am J Surg Pathol. 2006 Dec;30(12):1570-5
[
17122513.001
]
[Cites]
Arch Pathol Lab Med. 2007 Nov;131(11):1648-54
[
17979482.001
]
[Cites]
Lab Invest. 2008 Jan;88(1):78-88
[
18026163.001
]
[Cites]
Toxicology. 2008 Mar 20;245(3):194-205
[
18291570.001
]
[Cites]
Am J Clin Pathol. 2008 Aug;130(2):224-30
[
18628091.001
]
[Cites]
Arch Pathol Lab Med. 2008 Nov;132(11):1723-8
[
18976006.001
]
[Cites]
Biochem Biophys Res Commun. 2008 Dec 12;377(2):337-40
[
18831962.001
]
[Cites]
BMC Dev Biol. 2008;8:107
[
19000307.001
]
[Cites]
Int J Oncol. 2009 Mar;34(3):649-56
[
19212669.001
]
[Cites]
PLoS Pathog. 2009 Apr;5(4):e1000371
[
19360123.001
]
[Cites]
Acta Biochim Pol. 2009;56(3):465-9
[
19636440.001
]
[Cites]
J Pathol. 2009 Nov;219(3):365-72
[
19718708.001
]
[Cites]
Nitric Oxide. 2009 Nov-Dec;21(3-4):175-83
[
19638312.001
]
[Cites]
Mod Pathol. 2000 Aug;13(8):874-81
[
10955454.001
]
(PMID = 20661013.001).
[ISSN]
1532-0979
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK081417; United States / NIDDK NIH HHS / DK / R01 DK081417-01; United States / NIDDK NIH HHS / DK / R01 DK081417-02
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 3.5.3.1 / Arginase
[Other-IDs]
NLM/ NIHMS316258; NLM/ PMC3160135
17.
Liu SK, Yan C, Wu LL, Pan Y:
[Study strategies for neurobiology mechanism of "kidney storing will and responding to fear"].
Zhong Xi Yi Jie He Xue Bao
; 2010 Feb;8(2):106-10
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[Title]
[Study strategies for neurobiology mechanism of "
kidney
storing will and responding to fear"].
The theory of traditional Chinese medicine (TCM) deems that
kidney
essence is the material basis of formation, development and function of the brain and it maintains human being's psychomotility and behavior.
Moreover,
kidney
essence is the material basis of emotional activity.
The emotion theory in TCM deems that
kidney
stores will and responds to fear.
Combining the TCM theory with the modern psychological theory on stress, and from the points of views of the emotion regulation, the formation, consolidation, extraction and extinction of fear memory, and the plasticity of amygdala-hippocampus-prefrontal cortex nervous pathway, as well as the results of pharmacological studies of prescriptions and herbs for invigorating
the kidney
, the authors explained in this article the pathological mechanisms
of kidney
deficiency due to attack of fear, and revealed the material basis, the action modes, and the neurobiological mechanisms of the
kidney
in controlling and regulating emotional activity.
[MeSH-major]
Fear / physiology.
Kidney
/ physiology. Medicine, Chinese Traditional. Stress, Psychological
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.
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(PMID = 20141730.001).
[ISSN]
1672-1977
[Journal-full-title]
Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine
[ISO-abbreviation]
Zhong Xi Yi Jie He Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
18.
El-Husseini TK, Egail SA, Al-Orf AM, Mostert C:
Ossifying renal tumor of infancy.
Saudi Med J
; 2005 Dec;26(12):1978-9
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[Title]
Ossifying
renal tumor
of infancy.
Ossifying
renal tumor
of infancy ORTI is a
benign
neoplasm
, which presents with gross hematuria and less frequently as an abdominal mass, histologically it comprises a large cell with an epithelial nature and osteoid formation.
We report a case of a 10-month-old girl who developed ORTI as non-opacified upper calyces of left
kidney
on excretory urography.
We outlined the calcific and
tumors
nature of the lesion by ultrasound and computed tomography.
[MeSH-major]
Kidney Neoplasms
/ pathology.
Kidney Neoplasms
/ surgery. Ossification, Heterotopic / pathology. Ossification, Heterotopic / surgery
MedlinePlus Health Information.
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.
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(PMID = 16380785.001).
[ISSN]
0379-5284
[Journal-full-title]
Saudi medical journal
[ISO-abbreviation]
Saudi Med J
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Saudi Arabia
[Chemical-registry-number]
0 / Contrast Media
19.
Temmar M, Liabeuf S, Renard C, Czernichow S, Esper NE, Shahapuni I, Presne C, Makdassi R, Andrejak M, Tribouilloy C, Galan P, Safar ME, Choukroun G, Massy Z:
Pulse wave velocity and vascular calcification at different stages of chronic kidney disease.
J Hypertens
; 2010 Jan;28(1):163-9
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[Title]
Pulse wave velocity and vascular calcification at different stages of chronic
kidney
disease.
BACKGROUND: Increased arterial stiffness and vascular calcification have been recognized as important predictors of cardiovascular mortality in patients with chronic
kidney
disease.
METHOD: In order to examine the precise temporal link between aortic stiffness and cardiovascular risk at the earliest stages of chronic
kidney
disease, we studied a cohort of 150 patients with chronic
kidney
disease (52 stage 2/3 patients, 51 stage 4/5 patients and 47 stage 5D patients).
RESULTS: Regardless of the disease stage, patients with chronic
kidney
disease had higher adjusted pulse wave velocity than controls with preserved
renal
function (14.6 +/- 3.8 vs. 10.7 +/- 1.7 m/s, respectively; P < 0.0001).
Regarding aortic calcification, there was a gradual but significant rise in later chronic
kidney
disease stages.
CONCLUSION: We found that both vascular stiffness and vascular calcification appear early in patients with chronic
kidney
disease, but only vascular calcification worsens as the disease progresses.
The increase of vascular stiffness in adult patients with chronic
kidney
disease seems to be more related to age, systolic blood pressure, diabetes and vascular calcification than to uremic toxicity.
[MeSH-major]
Aorta, Abdominal / pathology. Aorta, Thoracic / pathology. Blood Circulation / physiology. Blood Pressure / physiology. Calcinosis / pathology.
Kidney
Failure, Chronic / pathology
Genetic Alliance.
consumer health - Kidney Disease
.
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consumer health - Kidney Failure
.
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(PMID = 19927012.001).
[ISSN]
1473-5598
[Journal-full-title]
Journal of hypertension
[ISO-abbreviation]
J. Hypertens.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
20.
Andratschke N, Schnaiter A, Weber WA, Cai L, Schill S, Wiedenmann N, Schwaiger M, Molls M, Nieder C:
Preclinical evaluation of erythropoietin administration in a model of radiation-induced kidney dysfunction.
Int J Radiat Oncol Biol Phys
; 2006 Apr 1;64(5):1513-8
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[Title]
Preclinical evaluation of erythropoietin administration in a model of radiation-induced
kidney
dysfunction.
PURPOSE: To test whether the clinically available growth factor erythropoietin (EPO) influences radiation-induced normal-tissue damage in a model
of kidney
dysfunction.
METHODS: Animal experiments were conducted to test the role of EPO administration in a C3H mouse model of unilateral
kidney
irradiation with 6, 8, and 10 Gy and to assess the effects of 2 different dose levels of EPO.
The kidney
function was assessed before radiotherapy, as well as 19, 25, 31, and 37 weeks thereafter by means of (99m)Tc-dimercaptosuccinat scans (static scintigraphy).
RESULTS: Concomitant EPO administration significantly increased the degree of radiation-induced
kidney
dysfunction.
CONCLUSION: Administration of growth factors concomitant to radiotherapy might modify the development
of kidney
dysfunction.
Although insulin-like growth factor-1 has previously been shown to protect
the kidney
, such an effect could not be demonstrated for EPO.
[MeSH-major]
Erythropoietin / adverse effects.
Kidney
/ radiation effects. Radiation Injuries, Experimental / prevention & control. Radiation Tolerance / drug effects
Hazardous Substances Data Bank.
EPOETIN ALFA
.
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[ErratumIn]
Int J Radiat Oncol Biol Phys. 2006 Jul 1;65(3):960. Schnaitera, Andrea [corrected to Schnaiter, Andrea]; Caia, Lu [corrected to Cai, Lu]
(PMID = 16580501.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Radiopharmaceuticals; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; 494JNQ8L28 / Technetium Tc 99m Dimercaptosuccinic Acid; 64FS3BFH5W / Epoetin Alfa
21.
Feltes CM, Van Eyk J, Rabb H:
Distant-organ changes after acute kidney injury.
Nephron Physiol
; 2008;109(4):p80-4
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[Title]
Distant-organ changes after acute
kidney
injury.
Acute
kidney
injury (AKI) contributes significantly to morbidity and mortality in both adults and children.
Leukocyte trafficking, cytokine expression, cell adhesion-molecule expression and membrane ion and water-channel expression in distant organs are deranged after
kidney
injury.
The responses to oxidative stress after AKI are also altered, suggesting complex mechanisms of crosstalk between the injured
kidney
and distant organs.
[MeSH-major]
Acute
Kidney
Injury / complications. Acute
Kidney
Injury / immunology. Cytokines / immunology. Models, Immunological. Multiple Organ Failure / complications. Multiple Organ Failure / immunology. Neutrophil Activation / immunology
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[Copyright]
Copyright 2008 S. Karger AG, Basel.
(PMID = 18802379.001).
[ISSN]
1660-2137
[Journal-full-title]
Nephron. Physiology
[ISO-abbreviation]
Nephron Physiol
[Language]
eng
[Grant]
United States / NHLBI NIH HHS / HV / N01 HV028180
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Cytokines
[Number-of-references]
26
22.
Cheng L, Williamson SR, Zhang S, Maclennan GT, Montironi R, Lopez-Beltran A:
Understanding the molecular genetics of renal cell neoplasia: implications for diagnosis, prognosis and therapy.
Expert Rev Anticancer Ther
; 2010 Jun;10(6):843-64
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[Title]
Understanding the molecular genetics of
renal
cell
neoplasia
: implications for
diagnosis
, prognosis and therapy.
Renal
neoplasms
exhibit a wide spectrum of molecular characteristics that are closely associated with their diverse morphologic manifestations and clinical behaviors.
A wealth of information has been garnered via methodology ranging from classical cytogenetics to FISH and gene expression profiling; however, the exact mechanisms by which each type of
renal tumor
develops remain incompletely understood.
Oddly,
tumors
with distinctly different morphology and prognosis sometimes show some overlap in the observed genetic abnormalities; by contrast, morphologically well characterized
benign
and malignant
tumors
that seem intuitively related cannot necessarily be shown to exhibit a step-wise progression from
benign
to malignant biologic behavior.
Nevertheless, modern methodologies have been highly successful, not only in subclassifying
renal
tumors
, but also in defining previously unrecognized entities.
We review the molecular and genetic characteristics of
renal
neoplasms
, with emphasis on markers that demonstrate utility in differentiating morphologically similar
neoplasms
and in predicting clinical outcome.
[MeSH-major]
Biomarkers,
Tumor
/ genetics. Carcinoma,
Renal
Cell /
diagnosis
. Carcinoma,
Renal
Cell / therapy.
Kidney Neoplasms
/
diagnosis
.
Kidney Neoplasms
/ therapy
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(PMID = 20553210.001).
[ISSN]
1744-8328
[Journal-full-title]
Expert review of anticancer therapy
[ISO-abbreviation]
Expert Rev Anticancer Ther
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor
[Number-of-references]
209
23.
Alie TM, Vrljicak PJ, Myburgh DB, Gupta IR:
Microinjection and electroporation of embryonic kidney explants: an improved method.
Kidney Int
; 2007 Jul;72(1):121-5
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[Title]
Microinjection and electroporation of embryonic
kidney
explants: an improved method.
Embryonic
kidney
explants are routinely used to study the molecular regulation
of kidney
development.
In this study, we show that a high voltage with a short pulse time is preferable for mouse
kidney
explants.
We suggest that our described conditions will make microinjection and electroporation a more effective method to study gene function in the developing mouse
kidney
.
[MeSH-major]
Electroporation / methods.
Kidney
/ embryology. Microinjections / methods
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(PMID = 17495853.001).
[ISSN]
0085-2538
[Journal-full-title]
Kidney international
[ISO-abbreviation]
Kidney Int.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
147336-22-9 / Green Fluorescent Proteins; EC 3.2.1.23 / beta-Galactosidase
24.
Argani P:
Metanephric neoplasms: the hyperdifferentiated, benign end of the Wilms tumor spectrum?
Clin Lab Med
; 2005 Jun;25(2):379-92
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[Title]
Metanephric
neoplasms
: the hyperdifferentiated,
benign
end of the Wilms
tumor
spectrum?
Metanephric
neoplasms
represent a spectrum of differentiated lesions that seem most likely to be related to Wilms
tumor
.
These
neoplasms
include a pure stromal lesion, a pure epithelial lesion (MA), and a mixed epithelial-stromal lesion (MAF).
The continuity of these lesions with Wilms
tumor
has been demonstrated best in the epithelial lesions.
The relationship of Wilms
tumor
, MAF with mitoses or combined MA/Wilms
tumor
lesions, and usual MAF or usual MA may be viewed as analogous to that of neuroblastoma, differentiating neuroblastoma, and ganglioneuroma, in which progressively more mature or differentiated counterparts of malignant embryonal lesions are associated with a greater probability of
benign
clinical behavior.
Such a spectrum already is recognized for cystic ILNR-derived nephroblastic lesions, ranging from cystic Wilms
tumor
, cystic partially differentiated nephroblastoma, and cystic nephroma.
Although this concept implies that the more active lesions (Wilms
tumor
) mature with time into inactive ones (usual MAFs or MA), the converse (that an active Wilms
tumor
can arise within an inactive usual MAF or MA) remains possible.
[MeSH-major]
Kidney Neoplasms
/ pathology. Wilms
Tumor
/ pathology
[MeSH-minor]
Adenofibroma / pathology. Adenoma / pathology. Carcinoma, Papillary / pathology. Carcinoma,
Renal
Cell / pathology.
Diagnosis
, Differential. Humans. Stromal Cells / pathology
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(PMID = 15848742.001).
[ISSN]
0272-2712
[Journal-full-title]
Clinics in laboratory medicine
[ISO-abbreviation]
Clin. Lab. Med.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
32
25.
Yang XJ, Zhou M, Hes O, Shen S, Li R, Lopez J, Shah RB, Yang Y, Chuang ST, Lin F, Tretiakova MM, Kort EJ, Teh BT:
Tubulocystic carcinoma of the kidney: clinicopathologic and molecular characterization.
Am J Surg Pathol
; 2008 Feb;32(2):177-87
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[Title]
Tubulocystic carcinoma of the
kidney
: clinicopathologic and molecular characterization.
The nature of tubulocystic carcinoma, a rare
renal tumor
composed of tubular and cystic structures, is poorly understood.
It has been suggested that it may represent a low-grade collecting duct carcinoma of the
kidney
despite the lack of sufficient molecular and pathologic evidence.
The aim of this study was to examine the clinical and pathologic features of 13 cases of tubulocystic carcinoma of the
kidney
.
Furthermore, using gene expression microarray analysis, we defined the molecular signature of this
tumor
by comparing it with other
renal
tumors
in our previously established molecular profile database.
Histologically, all 13
tumors
were composed of closely packed tubules and cysts of varying sizes separated by fibrovascular septa.
The epithelial lining cells of the tubules and cysts in this
tumor
were characterized by abundant eosinophilic cytoplasm with prominent nucleoli often showing a hobnail appearance.
Five of the 13 cases coexisted with papillary
renal
cell carcinoma (RCC) (n=3) or papillary adenoma (n=2).
Therefore, based on its unique pathologic features and molecular signature as well as its biologic behavior to develop metastasis either by itself or in association with papillary RCC, tubulocystic carcinoma of the
kidney
should be recognized as a distinct subtype of RCC and be distinguished from other malignant and
benign
cystic lesions of the
kidney
.
[MeSH-major]
Adenocarcinoma / pathology. Carcinoma,
Renal
Cell / secondary. Chromosome Aberrations. Cystadenocarcinoma / pathology.
Kidney Neoplasms
/ pathology
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Chromosomes, Human, Pair 17. Disease-Free Survival. Female. Fluorescent Antibody Technique, Indirect. Gene Expression Regulation, Neoplastic. Humans. Lymph Nodes / pathology. Male. Middle Aged.
Neoplasms
, Multiple Primary. Oligonucleotide Array Sequence Analysis
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(PMID = 18223319.001).
[ISSN]
0147-5185
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
26.
Costa MG, Garcia VD, Leirias MM, Santos SR, Oliveira DM:
Urgency priority in kidney transplantation in Rio Grande do Sul.
Transplant Proc
; 2007 Mar;39(2):381-2
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[Title]
Urgency priority in
kidney
transplantation in Rio Grande do Sul.
In 2002, it was established a system of urgency priority for
kidney
transplantations in cases with no vascular or peritoneal access for dialysis.
We reviewed cases of urgency priority request for
kidney
transplantation addressed to the CNCDO from May 2002 to August 2005.
Within this period the CNCDO received 35 urgency priority requests for
kidney
transplantation (mean, 1 every 1.2 months).
Among the 31 accepted, 26 (83%) had the transplantation performed in an average time of 19.6 days (range, 1-90), representing only 3.2% of all cadaveric
kidney
transplantations during that period.
[MeSH-major]
Kidney
Transplantation / statistics & numerical data. Tissue and Organ Procurement / statistics & numerical data. Waiting Lists
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(PMID = 17362736.001).
[ISSN]
0041-1345
[Journal-full-title]
Transplantation proceedings
[ISO-abbreviation]
Transplant. Proc.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
27.
Ahmadnia H, Shamsa A, Yarmohammadi A, Darabi M, Asl Zare M:
Kidney transplantation in older adults: does age affect graft survival?
Urol J
; 2005;2(2):93-6
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[Title]
Kidney
transplantation in older adults: does age affect graft survival?
INTRODUCTION: There is a paucity of data on long-term patient and graft survival in the older
kidney
recipients.
Our aim was to evaluate the long-term outcomes
of kidney
transplantation in patients aged 50 years and older and compare them with outcomes in younger recipients.
Patients who had received a cadaveric
kidney
allograft were excluded from the study.
CONCLUSION:
Kidney
transplantation should be considered in patients older than 50 years, since the graft survival rate is acceptable in this population, and early mortality and complications in this group are not different than those of younger recipients.
Although older patients have a shorter life expectancy, they benefit from
renal
transplantation in ways similar to younger
kidney
transplant recipients.
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(PMID = 17629878.001).
[ISSN]
1735-1308
[Journal-full-title]
Urology journal
[ISO-abbreviation]
Urol J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Iran
28.
Posadas MA, Yang V, Ho B, Omer M, Batlle D:
Acute renal failure and severe hypertension from a page kidney post-transplant biopsy.
ScientificWorldJournal
; 2010;10:1539-42
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[Title]
Acute
renal
failure and severe hypertension from a page
kidney
post-transplant biopsy.
Page
kidney
refers to a clinical picture characterized by acute onset of hypertension due to external compression of the
kidneys
from hematoma,
tumor
, lymphocele, or urinoma.
Hypertension is believed to result from renin-angiotensin-aldosterone activation triggered by
renal
hypoperfusion and microvascular ischemia.
Renal
failure, in addition to hypertension, may occur in the setting of a single functional
kidney
or a diseased contralateral
kidney
.
We report a case of a patient who had a transplant
kidney
biopsy complicated by a subcapsular perinephric hematoma.
The patient presented with an acute increase in blood pressure and a rapid rise in serum creatinine following a transplant
kidney
routine biopsy.
Early recognition and rapid intervention are needed in order to correct hypertension and reverse acute
renal
failure in Page
kidney
occurring in
renal
transplant recipients.
[MeSH-major]
Acute
Kidney
Injury / physiopathology. Hematoma / physiopathology. Hypertension / physiopathology.
Kidney
Transplantation / adverse effects
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(PMID = 20694451.001).
[ISSN]
1537-744X
[Journal-full-title]
TheScientificWorldJournal
[ISO-abbreviation]
ScientificWorldJournal
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
29.
Kinsey GR, Sharma R, Huang L, Li L, Vergis AL, Ye H, Ju ST, Okusa MD:
Regulatory T cells suppress innate immunity in kidney ischemia-reperfusion injury.
J Am Soc Nephrol
; 2009 Aug;20(8):1744-53
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[Title]
Regulatory T cells suppress innate immunity in
kidney
ischemia-reperfusion injury.
Both innate and adaptive mechanisms participate in the pathogenesis
of kidney
ischemia-reperfusion injury (IRI), but the role of regulatory immune mechanisms is unknown.
We hypothesized that the anti-inflammatory effects of CD4(+)CD25(+)FoxP3(+) regulatory T cells (Tregs) protect against
renal
IRI.
Partial depletion of Tregs with an anti-CD25 mAb potentiated
kidney
damage induced by IRI.
Reducing the number of Tregs resulted in more neutrophils, macrophages, and innate cytokine transcription in
the kidney
after IRI but did not affect CD4(+) T cells or B cells.
FoxP3(+) Treg-deficient mice accumulated a greater number of inflammatory leukocytes after
renal
IRI than mice containing Tregs.
To confirm that a lack of Tregs potentiated
renal
injury, we co-transferred isolated Tregs and Scurfy lymph node cells; Treg repletion significantly attenuated IRI-induced
renal
injury and leukocyte accumulation.
Furthermore, although adoptive transfer of wild-type Tregs into RAG-1 knockout mice was sufficient to prevent
kidney
IRI, transfer of IL-10-deficient Tregs was not.
Taken together, these results demonstrate that Tregs modulate injury after
kidney
IRI through IL-10-mediated suppression of the innate immune system.
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[Cites]
J Immunol. 2005 Aug 1;175(3):1965-73
[
16034141.001
]
[Cites]
Hum Immunol. 2005 Mar;66(3):222-30
[
15784460.001
]
[Cites]
J Am Soc Nephrol. 2005 Nov;16(11):3315-25
[
16192425.001
]
[Cites]
Trends Immunol. 2005 Dec;26(12):632-6
[
16243583.001
]
[Cites]
J Immunol. 2006 Mar 1;176(5):3108-14
[
16493070.001
]
[Cites]
Kidney Int. 2006 May;69(9):1601-8
[
16572108.001
]
[Cites]
Am J Physiol Renal Physiol. 2006 Jun;290(6):F1516-24
[
16403835.001
]
[Cites]
Nature. 2006 May 11;441(7090):235-8
[
16648838.001
]
[Cites]
J Immunol. 2006 Sep 1;177(5):3380-7
[
16920979.001
]
[Cites]
J Am Soc Nephrol. 2006 Oct;17(10):2731-41
[
16988067.001
]
[Cites]
J Immunol. 2006 Nov 15;177(10):6780-6
[
17082591.001
]
[Cites]
J Immunol. 2006 Nov 15;177(10):7155-63
[
17082633.001
]
[Cites]
J Leukoc Biol. 2007 Jan;81(1):144-53
[
16959895.001
]
[Cites]
Cancer Sci. 2007 Mar;98(3):416-23
[
17270031.001
]
[Cites]
J Autoimmun. 2006 Dec;27(4):289-96
[
17207605.001
]
[Cites]
J Immunol. 2007 Apr 1;178(7):4136-46
[
17371969.001
]
[Cites]
J Immunol. 2007 May 1;178(9):5899-911
[
17442974.001
]
[Cites]
J Autoimmun. 2007 Aug;29(1):10-9
[
17521882.001
]
[Cites]
Blood. 2007 Aug 15;110(4):1225-32
[
17449799.001
]
[Cites]
Nat Med. 2007 Oct;13(10):1248-52
[
17891146.001
]
[Cites]
J Immunol. 2008 Apr 1;180(7):4366-70
[
18354156.001
]
[Cites]
Eur J Immunol. 2008 Jun;38(6):1643-53
[
18493984.001
]
[Cites]
J Immunol. 2008 Sep 1;181(5):3524-34
[
18714025.001
]
[Cites]
J Immunol. 2008 Nov 15;181(10):6934-41
[
18981113.001
]
[Cites]
Infect Immun. 2008 Dec;76(12):5834-42
[
18824539.001
]
[Cites]
Kidney Int. 2008 Dec;74(12):1526-37
[
18843253.001
]
[Cites]
J Immunol. 2009 Jan 1;182(1):259-73
[
19109157.001
]
[Cites]
Kidney Int. 2009 Jan;75(2):167-75
[
18971925.001
]
[Cites]
Nat Med. 2009 Feb;15(2):192-9
[
19169263.001
]
[Cites]
J Leukoc Biol. 2008 Dec;84(6):1400-9
[
18765477.001
]
[Cites]
Annu Rev Immunol. 2001;19:683-765
[
11244051.001
]
[Cites]
J Clin Invest. 2001 Nov;108(9):1283-90
[
11696572.001
]
[Cites]
Kidney Int. 2001 Dec;60(6):2118-28
[
11737586.001
]
[Cites]
J Exp Med. 2002 Sep 16;196(6):851-7
[
12235217.001
]
[Cites]
J Immunol. 2002 Nov 1;169(9):4850-60
[
12391195.001
]
[Cites]
J Exp Med. 2003 Jan 6;197(1):111-9
[
12515818.001
]
[Cites]
Nat Immunol. 2003 Apr;4(4):330-6
[
12612578.001
]
[Cites]
Blood. 2003 Jul 1;102(1):328-35
[
12623845.001
]
[Cites]
Eur J Immunol. 2003 Aug;33(8):2090-7
[
12884282.001
]
[Cites]
J Immunol. 2003 Sep 15;171(6):3210-5
[
12960350.001
]
[Cites]
Arthritis Res Ther. 2004;6(5):215-22
[
15380036.001
]
[Cites]
J Clin Invest. 1996 Feb 15;97(4):1056-63
[
8613529.001
]
[Cites]
Am J Physiol. 1996 Mar;270(3 Pt 2):F500-9
[
8780254.001
]
[Cites]
J Immunol. 2005 Mar 1;174(5):2957-63
[
15728508.001
]
[Cites]
Am J Physiol Renal Physiol. 2005 Apr;288(4):F722-31
[
15561971.001
]
[Cites]
Nat Immunol. 2005 Nov;6(11):1142-51
[
16227984.001
]
(PMID = 19497969.001).
[ISSN]
1533-3450
[Journal-full-title]
Journal of the American Society of Nephrology : JASN
[ISO-abbreviation]
J. Am. Soc. Nephrol.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK62324; United States / NIAMS NIH HHS / AR / AR-051203; United States / NIDDK NIH HHS / DK / DK56223; United States / NIAMS NIH HHS / AR / R01 AR051203; United States / NIDCR NIH HHS / DE / DE-017579; United States / NIDDK NIH HHS / DK / R01 DK062324; United States / NIDDK NIH HHS / DK / R01 DK056223; United States / NIDDK NIH HHS / DK / T32 DK072922; United States / NIDDK NIH HHS / DK / DK58413; United States / NIDDK NIH HHS / DK / R44 DK058413; United States / NHLBI NIH HHS / HL / P01 HL073361; United States / NIDDK NIH HHS / DK / R41 DK058413
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Interleukin-2 Receptor alpha Subunit; 130068-27-8 / Interleukin-10
[Other-IDs]
NLM/ PMC2723989
30.
Karner CM, Chirumamilla R, Aoki S, Igarashi P, Wallingford JB, Carroll TJ:
Wnt9b signaling regulates planar cell polarity and kidney tubule morphogenesis.
Nat Genet
; 2009 Jul;41(7):793-9
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[Title]
Wnt9b signaling regulates planar cell polarity and
kidney
tubule morphogenesis.
Although many vertebrate organs, such as
kidneys
, lungs and liver, are composed of epithelial tubules, little is known of the mechanisms that establish the length or diameter of these tubules.
In
the kidney
, defects in the establishment or maintenance of tubule diameter are associated with one of the most common inherited human disorders, polycystic
kidney
disease.
Here we show that attenuation of Wnt9b signaling during
kidney
morphogenesis affects the planar cell polarity of the epithelium and leads to tubules with significantly increased diameter.
Although previous studies showed that polarized cell divisions maintain the diameter of postnatal
kidney
tubules, we find that cell divisions are randomly oriented during embryonic development.
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[Cites]
Lancet. 2007 Apr 14;369(9569):1287-301
[
17434405.001
]
[Cites]
J Am Soc Nephrol. 2007 May;18(5):1389-98
[
17429050.001
]
[Cites]
Development. 2007 Jul;134(13):2533-9
[
17537789.001
]
[Cites]
Dev Cell. 2007 Aug;13(2):214-25
[
17681133.001
]
[Cites]
Development. 2007 Sep;134(17):3049-54
[
17652351.001
]
[Cites]
Nat Rev Genet. 2007 Oct;8(10):791-802
[
17878895.001
]
[Cites]
Pediatr Nephrol. 2007 Nov;22(11):1825-38
[
17554566.001
]
[Cites]
Cell. 1998 Jul 10;94(1):109-18
[
9674432.001
]
[Cites]
Am J Physiol. 1999 Jul;277(1 Pt 2):F146-56
[
10409308.001
]
[Cites]
J Biol Chem. 2004 Dec 10;279(50):52703-13
[
15456783.001
]
[Cites]
Curr Biol. 2005 Apr 26;15(8):787-93
[
15854914.001
]
[Cites]
Nat Genet. 2005 May;37(5):537-43
[
15852005.001
]
[Cites]
Dev Cell. 2005 Aug;9(2):283-92
[
16054034.001
]
[Cites]
Nat Genet. 2005 Sep;37(9):980-5
[
16116426.001
]
[Cites]
EMBO J. 1999 Nov 1;18(21):5931-42
[
10545105.001
]
[Cites]
Development. 2000 May;127(10):2227-38
[
10769246.001
]
[Cites]
Nature. 2000 May 4;405(6782):76-81
[
10811221.001
]
[Cites]
Nature. 2000 May 4;405(6782):81-5
[
10811222.001
]
[Cites]
Development. 2000 Jul;127(14):3091-100
[
10862746.001
]
[Cites]
Nature. 2000 Sep 28;407(6803):527-30
[
11029006.001
]
[Cites]
Int J Dev Biol. 2001;45(1):225-7
[
11291850.001
]
[Cites]
Oncogene. 2001 Sep 20;20(42):5972-81
[
11593404.001
]
[Cites]
Am J Physiol Renal Physiol. 2002 Mar;282(3):F541-52
[
11832437.001
]
[Cites]
J Clin Invest. 2002 Feb;109(4):533-40
[
11854326.001
]
[Cites]
Dev Biol. 2002 Apr 15;244(2):305-18
[
11944939.001
]
[Cites]
Curr Biol. 2002 Jun 4;12(11):876-84
[
12062050.001
]
[Cites]
Curr Biol. 2002 Jun 4;12(11):R378-80
[
12062067.001
]
[Cites]
Dev Biol. 2002 Jul 1;247(1):165-81
[
12074560.001
]
[Cites]
J Am Soc Nephrol. 2002 Jul;13(7):1837-46
[
12089379.001
]
[Cites]
J Am Soc Nephrol. 2002 Oct;13(10):2508-16
[
12239239.001
]
[Cites]
Development. 2003 Jan;130(2):249-58
[
12466193.001
]
[Cites]
Nat Genet. 2007 Nov;39(11):1350-60
[
17906624.001
]
[Cites]
Development. 2007 Dec;134(23):4273-82
[
17978004.001
]
[Cites]
Nat Cell Biol. 2008 Jan;10(1):70-6
[
18084282.001
]
[Cites]
Dev Biol. 2008 Feb 1;314(1):112-26
[
18177851.001
]
[Cites]
PLoS One. 2008;3(4):e1964
[
18398480.001
]
[Cites]
Dev Biol. 2008 May 1;317(1):225-33
[
18384766.001
]
[Cites]
Hum Mol Genet. 2008 Jun 1;17(11):1578-90
[
18263895.001
]
[Cites]
Nat Genet. 2008 Aug;40(8):1010-5
[
18604206.001
]
[Cites]
J Cell Biol. 2008 Nov 3;183(3):377-84
[
18981227.001
]
[Cites]
Development. 2009 Jan;136(1):161-71
[
19060336.001
]
[Cites]
Nat Genet. 2003 Feb;33(2):129-37
[
12514735.001
]
[Cites]
Development. 2003 May;130(9):1725-34
[
12642479.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5286-91
[
12672950.001
]
[Cites]
Nat Genet. 2003 Aug;34(4):413-20
[
12872123.001
]
[Cites]
J Biol Chem. 2003 Sep 5;278(36):34211-8
[
12821668.001
]
[Cites]
Hum Mol Genet. 2003 Oct 15;12(20):2703-10
[
12925574.001
]
[Cites]
Development. 2004 Aug;131(16):4085-93
[
15269167.001
]
[Cites]
Nature. 2004 Aug 5;430(7000):689-93
[
15254551.001
]
[Cites]
Curr Opin Cell Biol. 2004 Oct;16(5):493-9
[
15363798.001
]
[Cites]
Kidney Int. 2004 Oct;66(4):1345-55
[
15458427.001
]
[Cites]
Nature. 1989 Mar 16;338(6212):263-4
[
2493583.001
]
[Cites]
Development. 1992 Dec;116(4):901-14
[
1295743.001
]
[Cites]
Genes Dev. 1994 Jan;8(1):118-30
[
8288125.001
]
[Cites]
Nature. 1997 May 15;387(6630):292-5
[
9153394.001
]
[Cites]
Nat Genet. 1997 Oct;17(2):179-81
[
9326937.001
]
[Cites]
Development. 1998 Mar;125(6):983-94
[
9463345.001
]
[Cites]
Cell. 2003 Jan 10;112(1):19-28
[
12526790.001
]
[Cites]
Genes Dev. 2003 Jan 15;17(2):295-309
[
12533515.001
]
[Cites]
Kidney Int. 2005 Nov;68(5):2010-8
[
16221201.001
]
[Cites]
Dev Biol. 2005 Dec 1;288(1):179-93
[
16277981.001
]
[Cites]
Nat Genet. 2006 Jan;38(1):21-3
[
16341222.001
]
[Cites]
Curr Biol. 2006 Jan 24;16(2):180-5
[
16431370.001
]
[Cites]
Curr Biol. 2006 Jan 24;16(2):186-94
[
16431371.001
]
[Cites]
Dev Cell. 2006 Mar;10(3):391-6
[
16516841.001
]
[Cites]
Curr Biol. 2006 Jun 20;16(12):1224-31
[
16782014.001
]
[Cites]
Semin Cell Dev Biol. 2006 Apr;17(2):194-203
[
16839790.001
]
[Cites]
Development. 2007 Jan;134(1):147-55
[
17164420.001
]
[Cites]
Differentiation. 2006 Dec;74(9-10):638-47
[
17177859.001
]
[Cites]
Blood. 2007 Feb 15;109(4):1345-52
[
17068148.001
]
[Cites]
Cell Cycle. 2007 Apr 1;6(7):776-9
[
17377490.001
]
(PMID = 19543268.001).
[ISSN]
1546-1718
[Journal-full-title]
Nature genetics
[ISO-abbreviation]
Nat. Genet.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / 5 P30 DK07403802; United States / NIDDK NIH HHS / DK / P30 DK074038; United States / NIDDK NIH HHS / DK / 1 R01 DK080004; United States / NIDDK NIH HHS / DK / R37 DK042921; United States / NIDDK NIH HHS / DK / P30 DK079328; United States / NIDDK NIH HHS / DK / DK074038-01; United States / NIDDK NIH HHS / DK / R01 DK080004; United States / NIDDK NIH HHS / DK / P30 DK074038-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Wnt Proteins; 0 / Wnt9b protein, mouse
[Other-IDs]
NLM/ NIHMS119253; NLM/ PMC2761080
31.
Torres PU:
[What are the actual indications for a surgical parathiroidectomy?].
Nephrol Ther
; 2005 Dec;1 Suppl 4:S342-50
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Secondary hyperparathyroidism (HPTH-II) is a major complication of chronic
renal
insufficiency (CRI).
Moreover, the hyperphosphaturia induced by PTH and its stimulant effect on calcitriol synthesis and tubular calcium reabsorption are compromised by the reduction in the expression of the
renal
PTH receptor.
The chronic stimulation of PTH by these anomalies causes progressive hyperplasia of the parathyroid cells which may be transformed into a
benign tumor
with a monoclonal appearance.
[MeSH-minor]
Humans. Incidence.
Kidney
Transplantation / physiology.
Renal
Dialysis / adverse effects
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(PMID = 17373206.001).
[ISSN]
1769-7255
[Journal-full-title]
Néphrologie & thérapeutique
[ISO-abbreviation]
Nephrol. Ther.
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
32.
Madi R, Wolf JS Jr:
Single-setting bilateral hand-assisted laparoscopic partial nephrectomy.
J Endourol
; 2009 Jun;23(6):929-32
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Renal
hilar clamping was not required, as the depth of penetration of all six
tumors
was only 0 to 4 mm (mean, 1.8 mm).
The
tumor
diameters ranged from 1.8 to 3.8 cm (mean, 2.4 cm).
Pathology revealed a
benign
lesion on one side and
renal
cell carcinoma on the other side in two patients, and bilateral leiomyomas in one patient.
CONCLUSION: Single-setting bilateral hand-assisted laparoscopic partial nephrectomies can be safely and effectively performed on patients with bilateral small exophytic
kidney tumors
.
We do not recommend this technique if both
kidneys
require temporary hilar occlusion, but it can be considered if only one
kidney
requires hilar occlusion.
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(PMID = 19473063.001).
[ISSN]
1557-900X
[Journal-full-title]
Journal of endourology
[ISO-abbreviation]
J. Endourol.
[Language]
ENG
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
33.
Arany I:
When less is more: apoptosis during acute kidney injury.
Kidney Int
; 2008 Aug;74(3):261-2
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[Title]
When less is more: apoptosis during acute
kidney
injury.
The paper by Ma and Devarajan suggests that the subtle apoptotic events that occur in the distal nephron after acute
kidney
injury might have a greater than expected impact on the adjacent proximal tubules and
kidney
function.
Understanding these events might facilitate development of therapeutic means to ameliorate acute
kidney
injury.
[MeSH-major]
Acute
Kidney
Injury / pathology. Apoptosis / physiology. Reperfusion Injury / pathology
[MeSH-minor]
Animals. Humans.
Kidney
/ physiopathology.
Kidney
Tubules, Proximal / physiopathology. Nephrons / physiopathology
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[CommentOn]
Kidney Int. 2008 Aug;74(3):310-8
[
18480747.001
]
(PMID = 18626494.001).
[ISSN]
1523-1755
[Journal-full-title]
Kidney international
[ISO-abbreviation]
Kidney Int.
[Language]
eng
[Publication-type]
Comment; Journal Article
[Publication-country]
United States
34.
Ciancio G, Burke GW 3rd:
Alemtuzumab (Campath-1H) in kidney transplantation.
Am J Transplant
; 2008 Jan;8(1):15-20
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[Title]
Alemtuzumab (Campath-1H) in
kidney
transplantation.
Kidney
transplantation has become the treatment of choice for both the quality of life and survival in patients with end-stage
renal
disease (ESRD).
However, the immunosuppressive regimen which allows optimal
kidney
transplant outcome remains elusive.
One of the more promising induction agents, Alemtuzumab, was introduced to
kidney
transplantation by Calne in the late 1990s with low dose cyclosporine A monotherapy, with the hope of establishing 'prope' or near tolerance.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use. Antibodies,
Neoplasm
/ therapeutic use. Graft Rejection / prevention & control. Immunosuppressive Agents / therapeutic use.
Kidney
Transplantation
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Kidney Transplantation
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 18093269.001).
[ISSN]
1600-6143
[Journal-full-title]
American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
[ISO-abbreviation]
Am. J. Transplant.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Review
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Immunosuppressive Agents; 3A189DH42V / alemtuzumab
[Number-of-references]
41
35.
Gómez-Ferrer Lozano A, Navarro Antón JA, Mola Arizo MJ, Polo i Peris AC:
[Erythrocytosis related with hydronephrosis in a horseshoe kidney].
Actas Urol Esp
; 2005 Apr;29(4):414-5
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[Title]
[Erythrocytosis related with hydronephrosis in a horseshoe
kidney
].
We report a case of a man with erythrocytosis secondary to hydronephrosis in a right horseshoe
kidney
.
Following nephrectomy of the right
kidney
erythrocyte count returned to normal values.
Secondary polyglobulia may be due to increased erythropoietine values and has been related in some patients with
renal
diseases such as hydronephrosis, but very rarely in association with hydronephrotic horseshoe
kidney
.
[MeSH-major]
Hydronephrosis / complications.
Kidney
/ abnormalities. Polycythemia / etiology
Genetic Alliance.
consumer health - Horseshoe kidney
.
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(PMID = 15981431.001).
[ISSN]
0210-4806
[Journal-full-title]
Actas urologicas espanolas
[ISO-abbreviation]
Actas Urol Esp
[Language]
spa
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Spain
36.
Kara C, Kutlu AO, Tosun MS, Apaydin S, Senel F:
Sertoli cell tumor causing prepubertal gynecomastia in a boy with peutz-jeghers syndrome: the outcome of 1-year treatment with the aromatase inhibitor testolactone.
Horm Res
; 2005;63(5):252-6
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[Title]
Sertoli cell
tumor
causing prepubertal gynecomastia in a boy with peutz-jeghers syndrome: the outcome of 1-year treatment with the aromatase inhibitor testolactone.
Peutz-Jeghers syndrome (PJS) is a rare
disorder
characterized by
benign
intestinal hamartomatous polyps and mucocutaneous pigmentation, and with an increased risk for intestinal and extra-intestinal
neoplasms
.
Sertoli cell
tumors
in boys with PJS have been increasingly recognized as a cause of prepubertal gynecomastia.
We report on a 7.25-year-old boy with PJS, bilateral gynecomastia, Sertoli cell
tumor
and nephrocalcinosis, and present the outcome of 1-year treatment with the aromatase inhibitor testolactone.
Histopathological examination was consistent with Sertoli cell
tumors
.
Nephrocalcinosis due to idiopathic
renal
hypercalciuria was also detected.
[MeSH-major]
Aromatase Inhibitors / therapeutic use. Gynecomastia / complications. Peutz-Jeghers Syndrome / complications. Sertoli Cell
Tumor
/ complications. Testicular
Neoplasms
/ complications. Testolactone / therapeutic use
Genetic Alliance.
consumer health - Peutz Jeghers syndrome
.
MedlinePlus Health Information.
consumer health - Testicular Cancer
.
Hazardous Substances Data Bank.
TESTOLACTONE
.
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(PMID = 15947469.001).
[ISSN]
0301-0163
[Journal-full-title]
Hormone research
[ISO-abbreviation]
Horm. Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Aromatase Inhibitors; 6J9BLA949Q / Testolactone
37.
Oh SJ, Lee SJ, Lee HY, Paik YH, Lee DK, Lee KS, Chung JB, Yu JS, Yoon DS:
[Extrapancreatic tumors in intraductal papillary mucinous neoplasm of the pancreas].
Korean J Gastroenterol
; 2009 Sep;54(3):162-6
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[Title]
[Extrapancreatic
tumors
in intraductal papillary mucinous
neoplasm of
the pancreas].
BACKGROUND/AIMS: Intraductal papillary mucinous
neoplasm
(IPMN) of the pancreas has a favorable prognosis, but seems to be associated with a high incidence of extrapancreatic
tumors
.
The purpose of this study was to evaluate the incidence and clinicopathological features of extrapancreatic
tumors
associated with IPMN.
These patients were examined for the development of extrapancreatic
tumors
.
RESULTS: Of 37 patients with IPMN, 14 (38%) had 18 extrapancreatic
tumors
, and 10 (27%) had 13 extrapancreatic malignancies.
Five, six, and two extrapancreatic malignancies had been diagnosed before, during, and after
the diagnosis
of IPMN.
Gastric adenocarcinoma (3 patients, 23%) and colorectal carcinoma (3 patients, 23%) were the most common
neoplasms
.
Other extrapancreatic
tumors
included lung cancer (n=2), prostatic cancer (n=1),
renal
cell carcinoma (n=1), cholangiocellular carcinoma (n=1), urinary bladder cancer (n=1), and gallbladder cancer (n=1), respectively.
As
benign tumor
, there were two gallbladder adenoma, one gastric adenoma, one colonic adenoma and one
benign
ovarian cystic
neoplasm
, respectively.
CONCLUSIONS: IPMN is associated with high incidence of extrapancreatic
tumors
, particularly gastric and colorectal
neoplasms
.
Upper gastrointestinal endoscopy and colonoscopy should be done, and systemic surveillance for the possible occurrence of other
tumors
may allow early detection of extrapancreatic
tumor
in patients with IPMN.
[MeSH-major]
Adenocarcinoma, Mucinous /
diagnosis
. Carcinoma, Pancreatic Ductal /
diagnosis
. Carcinoma, Papillary /
diagnosis
.
Neoplasms
, Multiple Primary / epidemiology.
Neoplasms
, Second Primary / epidemiology. Pancreatic
Neoplasms
/
diagnosis
MedlinePlus Health Information.
consumer health - Pancreatic Cancer
.
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[CommentIn]
Korean J Gastroenterol. 2009 Sep;54(3):196-8
[
19844158.001
]
(PMID = 19844152.001).
[ISSN]
1598-9992
[Journal-full-title]
The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
[ISO-abbreviation]
Korean J Gastroenterol
[Language]
kor
[Publication-type]
Journal Article
[Publication-country]
Korea (South)
38.
Rao PS, Ojo A:
The alphabet soup of kidney transplantation: SCD, DCD, ECD--fundamentals for the practicing nephrologist.
Clin J Am Soc Nephrol
; 2009 Nov;4(11):1827-31
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[Title]
The alphabet soup
of kidney
transplantation: SCD, DCD, ECD--fundamentals for the practicing nephrologist.
There is significant variability in the quality of deceased-donor
kidneys
that are used for transplantation.
The quality of the donor
kidney
has a direct effect on important clinical outcomes such as acute rejection, delayed graft function, and patient and allograft survival.
Expanded-criteria donors (ECDs) refer to older
kidney
donors (> or =60 yr) or donors who are aged 50 to 59 yr and have two of the following three features: Hypertension, terminal serum creatinine >1.5 mg/dl, or death from cerebrovascular accident.
By definition, ECD
kidneys
have a 70% greater likelihood of failure compared with one from a 35-yr-old male donor who died from a motor vehicle accident.
An ECD
kidney
transplant recipient has a projected average added-life-years of 5.1 yr compared with 10 yr for a
kidney
recipient from a standard-criteria donor.
Kidney
transplantation from DCD seems to have similar allograft and patient survival compared with
kidney
from donation after brain death; however DCD transplantation has a 42 to 51% risk for delayed graft function (need for at least one dialysis treatment during the first week after transplantation) compared with 24% in an standard-criteria donor
kidney
transplant.
Familiarity with the comprehensive allocation rules governing different categories of deceased-donor
kidneys
by the nephrologists and dialysis team providers is essential to maximizing patient autonomy and to improve the outcomes
of kidney
transplantation.
[MeSH-major]
Kidney
Transplantation. Nephrology. Tissue Donors. Tissue and Organ Procurement
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Kidney Transplantation
.
MedlinePlus Health Information.
consumer health - Organ Donation
.
COS Scholar Universe.
author profiles
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
The Lens.
Cited by Patents in
.
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(PMID = 19808229.001).
[ISSN]
1555-905X
[Journal-full-title]
Clinical journal of the American Society of Nephrology : CJASN
[ISO-abbreviation]
Clin J Am Soc Nephrol
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / K24 DK062234
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
24
39.
Tahvanainen E, Tahvanainen P, Kääriäinen H, Höckerstedt K:
Polycystic liver and kidney diseases.
Ann Med
; 2005;37(8):546-55
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[Title]
Polycystic liver and
kidney
diseases.
There have been remarkable advances in research on polycystic liver and
kidney
diseases recently, covering cloning of new genes, refining disease classifications, and advances in understanding more about the molecular pathology of these diseases.
Autosomal dominant polycystic
kidney
disease (ADPKD) is the most common hereditary disease affecting
kidneys
.
It affects 1/400 to 1/1000 live births and accounts for 5% of the end stage
renal
disease in the United States and Europe, and is caused by gene defects in the PKD1 or PKD2 genes.
Autosomal recessive polycystic
kidney
disease (ARPKD) belongs to a group of congenital hepatorenal fibrocystic syndromes.
[MeSH-major]
Cysts / genetics. Liver Diseases / genetics. Polycystic
Kidney
Diseases / genetics
[MeSH-minor]
Diagnosis
, Differential. Genetic Markers. Humans. Membrane Proteins / genetics. Proteins / genetics. TRPP Cation Channels
Genetics Home Reference.
consumer health - polycystic kidney disease
.
MedlinePlus Health Information.
consumer health - Liver Diseases
.
COS Scholar Universe.
author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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(PMID = 16338757.001).
[ISSN]
0785-3890
[Journal-full-title]
Annals of medicine
[ISO-abbreviation]
Ann. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Sweden
[Chemical-registry-number]
0 / Genetic Markers; 0 / Membrane Proteins; 0 / Proteins; 0 / SEC63 protein, human; 0 / TRPP Cation Channels; 0 / polycystic kidney disease 1 protein; 0 / polycystic kidney disease 2 protein
[Number-of-references]
95
40.
Cohen EP, Pais P, Moulder JE:
Chronic kidney disease after hematopoietic stem cell transplantation.
Semin Nephrol
; 2010 Nov;30(6):627-34
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[Title]
Chronic
kidney
disease after hematopoietic stem cell transplantation.
Acute and chronic
kidney
diseases occur after hematopoietic stem cell transplantation.
Recent estimates show that near 15% of subjects undergoing hematopoietic stem cell transplantation will develop chronic
kidney
disease, which is a complication rate that can affect outcome and reduce survival.
Investigation of the causes of chronic
kidney
disease is needed, as are ways to prevent, mitigate, and treat it.
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[Cites]
J Pathol. 2000 Mar;190(4):484-8
[
10699999.001
]
[Cites]
Curr Drug Targets. 2010 Nov;11(11):1423-9
[
20583975.001
]
[Cites]
Radiat Res. 2002 Apr;157(4):393-401
[
11893241.001
]
[Cites]
J Lab Clin Med. 2002 Apr;139(4):251-7
[
12024113.001
]
[Cites]
Am J Transplant. 2003 Mar;3(3):301-5
[
12614285.001
]
[Cites]
Blood. 2003 Oct 1;102(7):2695; author reply 2695-6
[
14504068.001
]
[Cites]
Pediatr Transplant. 2004 Oct;8(5):507-12
[
15367289.001
]
[Cites]
N Engl J Med. 1975 Apr 17;292(16):832-43
[
234595.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 1989 Jun;16(6):1501-9
[
2656600.001
]
[Cites]
Nephron. 1989;51(4):555-6
[
2662038.001
]
[Cites]
Kidney Int. 1989 Jun;35(6):1336-44
[
2671466.001
]
[Cites]
N Engl J Med. 1990 Feb 22;322(8):485-94
[
2300120.001
]
[Cites]
Ann Intern Med. 1991 Jan 15;114(2):113-8
[
1984385.001
]
[Cites]
Ann Intern Med. 1991 Dec 15;115(12):925-30
[
1952488.001
]
[Cites]
Nephron. 1993;64(4):626-35
[
8366991.001
]
[Cites]
N Engl J Med. 1994 Mar 24;330(12):827-38
[
8114836.001
]
[Cites]
Lab Invest. 1996 Sep;75(3):349-60
[
8804358.001
]
[Cites]
Lancet. 1998 Jan 17;351(9097):178-81
[
9449873.001
]
[Cites]
Bone Marrow Transplant. 1997 Dec;20(12):1069-74
[
9466280.001
]
[Cites]
Nephron. 1998 Aug;79(4):408-12
[
9689155.001
]
[Cites]
Int J Radiat Biol. 1999 Apr;75(4):473-9
[
10331853.001
]
[Cites]
Clin Transplant. 1999 Aug;13(4):330-5
[
10485375.001
]
[Cites]
Kidney Int Suppl. 2005 Aug;(97):S68-77
[
16014104.001
]
[Cites]
Br J Haematol. 2005 Oct;131(1):74-9
[
16173966.001
]
[Cites]
Am J Transplant. 2006 Jan;6(1):89-94
[
16433761.001
]
[Cites]
Bone Marrow Transplant. 2006 Sep;38(5):351-7
[
16862167.001
]
[Cites]
Semin Radiat Oncol. 2007 Apr;17(2):141-8
[
17395044.001
]
[Cites]
Bone Marrow Transplant. 2007 May;39(9):571-2
[
17351643.001
]
[Cites]
Nephrol Dial Transplant. 2007 May;22(5):1369-76
[
17255123.001
]
[Cites]
Bone Marrow Transplant. 2007 Jun;39(11):717-23
[
17401393.001
]
[Cites]
Medicine (Baltimore). 2007 Jul;86(4):215-24
[
17632263.001
]
[Cites]
Clin J Am Soc Nephrol. 2007 Sep;2(5):1014-23
[
17702721.001
]
[Cites]
Biol Blood Marrow Transplant. 2008 Apr;14(4):403-8
[
18342782.001
]
[Cites]
Int J Radiat Oncol Biol Phys. 2008 Apr 1;70(5):1546-51
[
18029109.001
]
[Cites]
Nephrology (Carlton). 2008 Jun;13(4):322-30
[
18221254.001
]
[Cites]
Biol Blood Marrow Transplant. 2008 Jun;14(6):658-63
[
18489991.001
]
[Cites]
Nephrol Dial Transplant. 2008 Aug;23(8):2700-1; author reply 2701
[
18385388.001
]
[Cites]
Cancer. 2008 Oct 1;113(7):1580-7
[
18704986.001
]
[Cites]
Am J Transplant. 2008 Nov;8(11):2378-90
[
18925905.001
]
[Cites]
Radiat Res. 2009 Feb;171(2):164-72
[
19267541.001
]
[Cites]
Radiat Res. 2009 Aug;172(2):260-4
[
19630531.001
]
[Cites]
Biol Blood Marrow Transplant. 2009 Oct;15(10):1251-7
[
19747632.001
]
[Cites]
Transplant Proc. 2009 Sep;41(7):2895-7
[
19765466.001
]
[Cites]
Nephrol Dial Transplant. 2010 Jan;25(1):278-82
[
19762604.001
]
[Cites]
Kidney Int. 2010 Feb;77(3):219-24
[
19940841.001
]
[Cites]
Bone Marrow Transplant. 2010 Feb;45(2):219-34
[
19584824.001
]
[Cites]
Exp Hematol. 2010 Apr;38(4):270-81
[
20116413.001
]
[Cites]
Clin J Am Soc Nephrol. 2010 Jun;5(6):1107-13
[
20299374.001
]
[Cites]
Clin Transplant. 2010 Jul-Aug;24(4):E94-102
[
19919608.001
]
[Cites]
Radiat Res. 2001 Mar;155(3):474-80
[
11182799.001
]
(PMID = 21146127.001).
[ISSN]
1558-4488
[Journal-full-title]
Seminars in nephrology
[ISO-abbreviation]
Semin. Nephrol.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / U19 AI067734; United States / NIAID NIH HHS / AI / 1U19AI067734
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS249843; NLM/ PMC3005300
41.
Kim SS, Park HJ, Han J, Gwak SJ, Park MH, Song KW, Rhee YH, Min Chung H, Kim BS:
Improvement of kidney failure with fetal kidney precursor cell transplantation.
Transplantation
; 2007 May 15;83(9):1249-58
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[Title]
Improvement
of kidney
failure with fetal
kidney
precursor cell transplantation.
BACKGROUND: Current therapies for end-stage
renal
disease have severe limitations.
Dialysis is only a temporary treatment and does not restore
kidney
function.
Here, we show that the transplantation of fetal
kidney
precursor cells reconstitutes
kidney
tissues, reduces uremic symptoms, and provides life-saving metabolic support in
kidney
failure animal models.
METHODS:
Kidney
failure was surgically induced by resecting
kidneys
, leaving approximately 1/6 of the total
kidney
mass (5/6 nephrectomy).
Fetal
kidney
precursor cells were isolated from metanephroi of E17.5 rat fetuses using collagenase/dispase digestion.
Five weeks after the nephrectomy procedure, isolated fetal
kidney
precursor cells were transplanted under
the kidney
capsule of rats using fibrin gel matrix.
The cell transplantation into
the kidneys of kidney
failure-induced rats resulted in
kidney
tissue reconstitution and the transplanted cells were observed in the reconstitution region of the
kidneys
as evidenced by the presence of fluorescently labeled cells.
In addition, biochemical parameters from serum and urine samples showed improved
kidney
functions compared with non-treated group without severe immune response after ten weeks.
CONCLUSION: Transplanting fetal
kidney
precursor cells showed the potential for the partial augmentation
of kidney
structure and function in the treatment
of kidney
failure.
[MeSH-major]
Embryonic Stem Cells / transplantation.
Renal
Insufficiency / physiopathology.
Renal
Insufficiency / surgery
[MeSH-minor]
Animals. Cell Membrane. Disease Models, Animal. Disease Progression. Disease Susceptibility. Glomerulosclerosis, Focal Segmental / pathology. Glomerulosclerosis, Focal Segmental / physiopathology. Graft Rejection / etiology. Hypertrophy.
Kidney
/ pathology.
Kidney
/ physiopathology.
Kidney
Glomerulus / pathology.
Kidney
Glomerulus / physiopathology. Nephrectomy. Phenotype. Rats. Rats, Sprague-Dawley. Regeneration. Survival Analysis. Uremia / physiopathology
The Lens.
Cited by Patents in
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(PMID = 17496543.001).
[ISSN]
0041-1337
[Journal-full-title]
Transplantation
[ISO-abbreviation]
Transplantation
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
42.
Schaeffner ES, Födinger M, Kramar R, Frei U, Hörl WH, Sunder-Plassmann G, Winkelmayer WC:
Prognostic associations between lipid markers and outcomes in kidney transplant recipients.
Am J Kidney Dis
; 2006 Mar;47(3):509-17
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[Title]
Prognostic associations between lipid markers and outcomes in
kidney
transplant recipients.
BACKGROUND: Hyperlipidemia is highly prevalent in
kidney
transplant recipients, but the prognostic significance for mortality and allograft survival in these patients has not been established sufficiently.
METHODS: We prospectively enrolled 733
kidney
transplant recipients between 1996 and 1998.
Using multivariate proportional hazard regression, independent relations of fasting plasma triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol levels to risk for death from any cause and risk for
kidney
allograft loss were examined.
RESULTS: During a median follow-up of 6.1 years, 154 patients died and 260
kidney
allografts were lost.
Further analysis of associations between high-density lipoprotein cholesterol or low-density lipoprotein cholesterol categories and patient mortality or
kidney
allograft loss did not show associations.
CONCLUSION: Elevated levels of TC or its subfractions and elevated TG levels are not associated with increased risk for patient mortality or allograft loss in these
kidney
transplant recipients.
[MeSH-major]
Cholesterol / blood. Graft Survival.
Kidney
Transplantation
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CHOLESTEROL
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(PMID = 16490631.001).
[ISSN]
1523-6838
[Journal-full-title]
American journal of kidney diseases : the official journal of the National Kidney Foundation
[ISO-abbreviation]
Am. J. Kidney Dis.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers; 0 / Triglycerides; 97C5T2UQ7J / Cholesterol
43.
Hostanska K, Suter A, Melzer J, Saller R:
Evaluation of cell death caused by an ethanolic extract of Serenoae repentis fructus (Prostasan) on human carcinoma cell lines.
Anticancer Res
; 2007 Mar-Apr;27(2):873-81
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BACKGROUND: Phytotherapy is a third approach for treating lower urinary tract symptoms associated with
benign
prostatic hyperplasia (BPH).
MATERIALS AND METHODS: The effect of an ethanolic extract of S. repens (10-1000 microg/ml) was tested in hormone-sensitive LNCaP, MCF-7 and hormone-insensitive
DU
145, MDA MB231 prostate, breast carcinoma cell lines,
renal
Caki-1, urinary bladder J82, colon HCT 116 and lung A 549 cancer cells.
In hormone-sensitive prostate LNCaP and breast MCF-7 cell lines, the effect of extract expressed in GI50 was 2.2- and 2.5-fold more potent (p < 0.01) than in hormone-insensitive
DU
145 and MDA MB231 cells.
[MeSH-major]
Apoptosis / drug effects. Fruit / chemistry.
Neoplasms
/ drug therapy. Phytotherapy / methods. Plant Extracts / pharmacology. Serenoa / chemistry
[MeSH-minor]
Breast
Neoplasms
/ drug therapy. Cell Line,
Tumor
. Drug Screening Assays, Antitumor. Female. HCT116 Cells. Humans. Male.
Neoplasms
, Hormone-Dependent / drug therapy. Prostatic
Neoplasms
/ drug therapy
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(PMID = 17465214.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Plant Extracts
44.
Paleologo G, Abdelkawy H, Barsotti M, Basha A, Bernabini G, Bianchi A, Caprio F, Emad A, Grassi G, Nerucci B, Tregnaghi C, Rizzo G, Donadio C:
Kidney dimensions at sonography are correlated with glomerular filtration rate in renal transplant recipients and in kidney donors.
Transplant Proc
; 2007 Jul-Aug;39(6):1779-81
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[Title]
Kidney
dimensions at sonography are correlated with glomerular filtration rate in
renal
transplant recipients and in
kidney
donors.
The gold standard to assess
renal
function is the measurement of glomerular filtration rate (GFR).
For practical reasons,
renal
function is often evaluated from serum creatinine (S Cr) or cystatin C (S Cys), and GFR is predicted from SCr.
Ultrasound scanning of the
kidneys
is used only to evaluate
renal
morphology.
The aim of this study was to evaluate the relationship between sonographic
renal
dimensions and GFR in
renal
transplant recipients and in
kidney
donors.
GFR was also predicted using the Cockcroft and Gault (CG) formula and with the simplified Modification of Diet in
Renal
Disease (MDRD) formula.
Length, width, and depth
of kidneys
and
renal
sinus were measured using
renal
sonography.
Among sonographic measurements,
kidney
length showed the best correlation with GFR.
In either case, the correlation
of kidney
length with GFR was greater than that of S Cr or S Cys, and similar to that of CG or MDRD GFR.
Accuracy
of kidney
length as an indicator of GFR impairment was not statistically different from laboratory tests.
In conclusion,
renal
dimensions at sonography closely correlated with GFR.
Thus,
renal
sonography can give information also on the function of the
renal
graft and of the remaining
kidney of
living donors.
[MeSH-major]
Glomerular Filtration Rate.
Kidney
/ anatomy & histology.
Kidney
/ physiology.
Kidney
Transplantation / physiology. Tissue Donors
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(PMID = 17692610.001).
[ISSN]
0041-1345
[Journal-full-title]
Transplantation proceedings
[ISO-abbreviation]
Transplant. Proc.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers; 0 / CST3 protein, human; 0 / Cystatin C; 0 / Cystatins; AYI8EX34EU / Creatinine
45.
Zhuang WL, Wu YM, Ge SY, Mei CL:
[Detection of differentially expressed genes in human autosomal dominant polycystic kidney tissue].
Zhonghua Yi Xue Yi Chuan Xue Za Zhi
; 2005 Dec;22(6):705-8
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[Title]
[Detection of differentially expressed genes in human autosomal dominant polycystic
kidney
tissue].
OBJECTIVE: To detect the differentially expressed genes in human polycystic
kidney
by cDNA microarray.
Both mRNAs isolated from polycystic
kidney
tissue and normal
kidney
tissue were reversely transcribed to cDNAs with the incorporation of fluorescent dUTP (Cy5-dUTP and Cy3-dUTP) for preparing the hybridization probes.
RESULTS: The result indicated that the expressions of 263 genes were up regulated while the expressions of 94 genes were down regulated in the polycystic
kidney
tissue among the 8398 target genes.
Three hundred and fifty-seven differentially expressed genes with different functions were revealed in the polycystic
kidney
tissue, which may play some roles in the progression of polycystic
kidney
.
[MeSH-major]
Gene Expression Profiling. Oligonucleotide Array Sequence Analysis / methods. Polycystic
Kidney
, Autosomal Dominant / genetics
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(PMID = 16331579.001).
[ISSN]
1003-9406
[Journal-full-title]
Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
[ISO-abbreviation]
Zhonghua Yi Xue Yi Chuan Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Carbocyanines; 0 / DNA, Complementary; 0 / Fluorescent Dyes; 0 / cyanine dye 3; 0 / cyanine dye 5; 67763-96-6 / Insulin-Like Growth Factor I
46.
Otsuka M, Ambiru S, Uryuhara K, Herman P, Talpe S, Dehoux JP, Jamar F, Gianello P:
Early biological and immune response to semi-identical liver or kidney allograft in miniature swine.
Transpl Int
; 2005 Jan;18(1):78-88
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[Title]
Early biological and immune response to semi-identical liver or
kidney
allograft in miniature swine.
In inbred miniature swine, semi-identical liver allograft recipients survive up to 3 months without immunosuppression, whereas similarly mismatched
kidney
allografts are uniformly rejected within 2 weeks.
SLA(d/d) pigs (MGH, Harvard Medical School, Boston, MA, USA) received liver or
kidney
allograft from heterozygous SLA(c/d) miniature swine.
Kidney
allografts were uniformly rejected within 2 weeks, whereas liver allografts survived for up to 87 days.
After both liver and
kidney
transplantation, the peripheral lymphocyte count decreased during the first week concomitantly to a significant elevation of plasma cortisol level.
Early decrease of peripheral platelet count was observed after liver but not
renal
transplantation.
Up-regulation of transforming growth factor beta1 (TGF-beta1) and interferon-gamma (IFN-gamma) was observed during the first postoperative week in semi-identical liver allografts and IFN-gamma as well as IL-10 in
kidney
allografts.
In liver recipients, labelled autologous lymphocytes accumulated in the liver graft and native spleen, whereas after
renal
allograft, lymphocytes accumulated in the native spleen and liver but never in
the kidney
allograft.
Specific cellular anti-donor unresponsiveness was observed from the first post-transplant day in both liver and
kidney
recipients, while the humoral anti-donor response remained intact.
In semi-identical liver allograft, recipient rejection is milder and slower than in similarly matched
kidney
allograft.
The rapid, nonspecific accumulation of recipient lymphocytes in the liver allograft but not in
kidney
allograft might also play a role in the different survival time in this model.
[MeSH-major]
Kidney
Transplantation / physiology. Liver Transplantation / physiology
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(PMID = 15612988.001).
[ISSN]
0934-0874
[Journal-full-title]
Transplant international : official journal of the European Society for Organ Transplantation
[ISO-abbreviation]
Transpl. Int.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Cytokines; 0 / DNA Primers; 0 / RNA, Messenger
47.
Lin F:
Stem cells in kidney regeneration following acute renal injury.
Pediatr Res
; 2006 Apr;59(4 Pt 2):74R-8R
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[Title]
Stem cells in
kidney
regeneration following acute
renal
injury.
Acute
renal
failure has 50-80% mortality.
Stem cells offer an exciting potential for
kidney
regeneration.
This review discusses pathogenesis of acute
renal
failure resulting from ischemia-reperfusion injury and the role of stem cells in reversing or mitigating this
disorder
.
Specifically, the issues of differentiation
of kidney
cells from embryonic stem cells and bone marrow stem cells, and whether adult
kidney
stem/progenitor cells exist in the postnatal
kidney
are discussed.
Evidence to support the conclusion that intra-
renal
cells, including surviving tubular epithelial cells and potential
renal
stem/progenitor cells, are the main source for
renal
regeneration is provided.
Future research in selecting the type(s) of stem cells and optimizing the dose, frequency and route of administration of the cells will be fundamental in successful cell replacement therapy in acute
renal
failure.
Methods for enhancing endogenous
renal
cell proliferation and differentiation for
renal
repair continue to be important research directions.
[MeSH-major]
Kidney
/ physiopathology. Regeneration. Stem Cells / cytology
[MeSH-minor]
Bone Marrow Cells / cytology. Cell Differentiation. Humans.
Renal
Insufficiency / physiopathology.
Renal
Insufficiency / therapy
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(PMID = 16549552.001).
[ISSN]
0031-3998
[Journal-full-title]
Pediatric research
[ISO-abbreviation]
Pediatr. Res.
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / K08 DK062839; United States / NIDDK NIH HHS / DK / R01 DK66535
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
48
48.
Masoumi A, Reed-Gitomer B, Kelleher C, Schrier RW:
Potential pharmacological interventions in polycystic kidney disease.
Drugs
; 2007;67(17):2495-510
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[Title]
Potential pharmacological interventions in polycystic
kidney
disease.
Polycystic
kidney
diseases (autosomal dominant and autosomal recessive) are progressive
renal
tubular cystic diseases, which are characterised by cyst expansion and loss of normal
kidney
structure and function.
Autosomal dominant polycystic
kidney
disease (ADPKD) is the most common life- threatening, hereditary disease.
Early
diagnosis
and treatment of hypertension with inhibitors of the renin-angiotensin-aldosterone system (RAAS) and its potential protective effect on left ventricular hypertrophy has been one of the major therapeutic goals to decrease cardiac complications and contribute to improved prognosis of the disease.
Because of activation of the mammalian target of rapamycin (mTOR) pathway, the use of sirolimus (rapamycin) an mTOR inhibitor, markedly reduced cyst formation and decreased polycystic
kidney
size in several animal models.
Caspase inhibitors have been shown to decrease cytogenesis and
renal
failure in rats with cystic disease.
Cystic fluid secretion results in cyst enlargement and somatostatin analogues have been shown to decrease
renal
cyst progression in patients with ADPKD.
[MeSH-major]
Polycystic
Kidney
Diseases / drug therapy
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[Cites]
J Am Soc Nephrol. 2006 Aug;17(8):2220-7
[
16807403.001
]
[Cites]
Kidney Int. 2002 Apr;61(4):1220-30
[
11918728.001
]
[Cites]
Adv Cancer Res. 2000;77:25-79
[
10549355.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7037-44
[
11416184.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jul 9;99(14):9260-5
[
12082174.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):13254-9
[
12239346.001
]
[Cites]
Mamm Genome. 2003 Apr;14(4):242-9
[
12682776.001
]
[Cites]
J Am Soc Nephrol. 1997 Aug;8(8):1292-7
[
9259356.001
]
[Cites]
Science. 1998 Apr 3;280(5360):32-4
[
9556450.001
]
[Cites]
Mol Cell Biol. 2002 Jul;22(14):4984-96
[
12077328.001
]
[Cites]
Kidney Int. 1991 Jan;39(1):57-62
[
2002633.001
]
[Cites]
Cell Signal. 2003 May;15(5):463-9
[
12639709.001
]
[Cites]
Biochem Biophys Res Commun. 2001 Mar 23;282(1):341-50
[
11264013.001
]
[Cites]
Am J Physiol. 1991 Dec;261(6 Pt 2):F951-6
[
1661085.001
]
[Cites]
Cell Signal. 1999 Sep;11(9):651-63
[
10530873.001
]
[Cites]
J Am Soc Nephrol. 2001 Feb;12(2):379-84
[
11158230.001
]
[Cites]
Kidney Int. 1996 Oct;50(4):1327-36
[
8887295.001
]
[Cites]
Am J Kidney Dis. 1994 Oct;24(4):561-8
[
7942810.001
]
[Cites]
Am J Physiol. 1995 Aug;269(2 Pt 1):C487-95
[
7653531.001
]
[Cites]
J Clin Invest. 1997 Mar 15;99(6):1380-9
[
9077548.001
]
[Cites]
J Biol Chem. 2001 Jun 8;276(23):20451-7
[
11278652.001
]
[Cites]
J Pharmacol Exp Ther. 1995 Feb;272(2):546-51
[
7853167.001
]
[Cites]
Biochem Biophys Res Commun. 2004 Oct 1;322(4):1374-83
[
15336986.001
]
[Cites]
Kidney Int. 2004 Sep;66(3):964-73
[
15327388.001
]
[Cites]
Dev Cell. 2003 May;4(5):753-9
[
12737809.001
]
[Cites]
Kidney Int. 1989 Feb;35(2):675-80
[
2709672.001
]
[Cites]
Adv Nephrol Necker Hosp. 1998;28:439-78
[
9890004.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1432-7
[
9465032.001
]
[Cites]
Kidney Int. 2005 Mar;67(3):909-19
[
15698430.001
]
[Cites]
J Am Soc Nephrol. 2002 Sep;13(9):2384-98
[
12191984.001
]
[Cites]
FASEB J. 2001 Nov;15(13):2536-8
[
11641256.001
]
[Cites]
J Cell Biochem. 2002;86(1):21-8
[
12112012.001
]
[Cites]
Curr Biol. 2002 Jun 4;12(11):R378-80
[
12062067.001
]
[Cites]
Crit Rev Oncol Hematol. 2000 Jan;33(1):7-23
[
10714959.001
]
[Cites]
Methods. 2003 Jul;30(3):191-7
[
12798133.001
]
[Cites]
Kidney Int. 1999 Jan;55(1):29-62
[
9893113.001
]
[Cites]
J Urol. 1998 Jan;159(1):291-6
[
9400497.001
]
[Cites]
J Am Soc Nephrol. 2003 Feb;14 (2):367-76
[
12538737.001
]
[Cites]
Am J Physiol Renal Physiol. 2003 Nov;285(5):F998-F1012
[
12837680.001
]
[Cites]
J Am Soc Nephrol. 2000 Jul;11(7):1179-87
[
10864573.001
]
[Cites]
Clin Cancer Res. 1998 Apr;4(4):821-8
[
9563874.001
]
[Cites]
Kidney Int. 2000 Apr;57(4):1460-71
[
10760082.001
]
[Cites]
Pediatrics. 2003 May;111(5 Pt 1):1072-80
[
12728091.001
]
[Cites]
Biochem Biophys Res Commun. 1993 Dec 30;197(3):1083-93
[
8280123.001
]
[Cites]
J Am Soc Nephrol. 1993 Jan;3(7):1378-86
[
8094982.001
]
[Cites]
J Membr Biol. 2001 Nov 1;184(1):71-9
[
11687880.001
]
[Cites]
J Biol Chem. 2004 Jul 9;279(28):29728-39
[
15123714.001
]
[Cites]
Nat Genet. 2005 May;37(5):537-43
[
15852005.001
]
[Cites]
Circulation. 2001 May 15;103(19):2387-94
[
11352889.001
]
[Cites]
Kidney Int. 2005 Jul;68(1):206-16
[
15954910.001
]
[Cites]
Kidney Int. 1988 Nov;34(5):683-90
[
2974094.001
]
[Cites]
Am J Kidney Dis. 1996 Dec;28(6):788-803
[
8957030.001
]
[Cites]
Am J Kidney Dis. 1997 Nov;30(5):703-9
[
9370187.001
]
[Cites]
Pol Arch Med Wewn. 1996 Oct;96(4):329-43
[
9082344.001
]
[Cites]
Physiol Rev. 1998 Oct;78(4):1165-91
[
9790573.001
]
[Cites]
Cell. 2004 Jun 11;117(6):693-7
[
15186771.001
]
[Cites]
J Clin Invest. 2000 Jan;105(1):9-13
[
10619855.001
]
[Cites]
Am J Physiol Renal Physiol. 2004 Oct;287(4):F775-88
[
15187005.001
]
[Cites]
J Pediatr. 1987 May;110(5):729-34
[
2883274.001
]
[Cites]
Kidney Int. 1992 Jan;41(1):206-10
[
1317477.001
]
[Cites]
J Clin Invest. 1998 Mar 1;101(5):935-9
[
9486961.001
]
[Cites]
Kidney Int. 2005 Apr;67(4):1234-47
[
15780076.001
]
[Cites]
J Cell Sci. 2003 Apr 15;116(Pt 8):1519-25
[
12640036.001
]
[Cites]
J Am Soc Nephrol. 2002 Oct;13(10):2508-16
[
12239239.001
]
[Cites]
Kidney Int. 1992 Aug;42(2):364-73
[
1405319.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Jan 20;95(2):554-9
[
9435230.001
]
[Cites]
J Clin Invest. 2002 Oct;110(8):1083-91
[
12393844.001
]
[Cites]
Semin Nephrol. 1991 Nov;11(6):653-60
[
1767138.001
]
[Cites]
Nat Genet. 2003 Feb;33(2):129-37
[
12514735.001
]
[Cites]
J Am Soc Nephrol. 1993 Oct;4(4):1064-72
[
7904485.001
]
[Cites]
Kidney Int. 1988 Jun;33(6):1084-90
[
3043076.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5286-91
[
12672950.001
]
[Cites]
J Biol Chem. 2001 Mar 9;276(10):7320-6
[
11058599.001
]
[Cites]
Am J Physiol Renal Physiol. 2002 Dec;283(6):F1313-25
[
12388409.001
]
[Cites]
Trends Cell Biol. 2004 Feb;14 (2):78-85
[
15102439.001
]
[Cites]
Oncogene. 1999 Nov 11;18(47):6505-12
[
10597253.001
]
[Cites]
J Am Soc Nephrol. 2005 Jan;16(1):46-51
[
15563559.001
]
[Cites]
Am J Physiol. 1998 Sep;275(3 Pt 2):F387-94
[
9729511.001
]
[Cites]
Hum Mol Genet. 2003 Aug 1;12(15):1875-80
[
12874107.001
]
[Cites]
Nat Genet. 1995 Jun;10(2):151-60
[
7663510.001
]
[Cites]
Nat Med. 2004 Apr;10(4):363-4
[
14991049.001
]
[Cites]
Circ Res. 2005 Apr 29;96(8):873-80
[
15790956.001
]
[Cites]
FASEB J. 2004 May;18(7):884-6
[
15001556.001
]
[Cites]
Curr Biol. 2001 May 1;11(9):R356-60
[
11369247.001
]
[Cites]
Mayo Clin Proc. 1991 Oct;66(10):1010-7
[
1921483.001
]
[Cites]
J Clin Invest. 2004 Mar;113(6):814-25
[
15067314.001
]
[Cites]
Oncogene. 1998 Sep 17;17(11 Reviews):1395-413
[
9779987.001
]
[Cites]
J Anat. 2001 Oct;199(Pt 4):393-405
[
11693300.001
]
[Cites]
J Am Soc Nephrol. 2005 Apr;16(4):846-51
[
15728778.001
]
[Cites]
N Engl J Med. 2004 Jan 8;350(2):151-64
[
14711914.001
]
[Cites]
J Am Soc Nephrol. 2002 Nov;13(11):2723-9
[
12397042.001
]
[Cites]
J Biol Chem. 1997 Jul 18;272(29):17907-11
[
9218414.001
]
[Cites]
J Biol Chem. 2000 Oct 13;275(41):31921-9
[
10931830.001
]
[Cites]
Mol Cell Biol. 1999 May;19(5):3423-34
[
10207066.001
]
[Cites]
Kidney Int. 2003 Nov;64(5):1792-9
[
14531813.001
]
[Cites]
Am J Kidney Dis. 1995 Sep;26(3):501-7
[
7645559.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 May 25;96(11):6241-8
[
10339572.001
]
[Cites]
Trends Biochem Sci. 2004 Jan;29(1):32-8
[
14729330.001
]
[Cites]
Lab Invest. 1974 Oct;31(4):303-13
[
4412080.001
]
[Cites]
Hum Mol Genet. 2003 Oct 15;12(20):2703-10
[
12925574.001
]
[Cites]
Dev Biol. 1990 Mar;138(1):225-30
[
1968405.001
]
[Cites]
Am J Nephrol. 1985;5(3):176-81
[
3893129.001
]
[Cites]
J Am Soc Nephrol. 1994 Dec;5(6):1349-54
[
7894001.001
]
[Cites]
Nephron. 1979;24(4):198-204
[
40149.001
]
[Cites]
Cancer Res. 1995 Jan 15;55(2):354-9
[
7812968.001
]
[Cites]
J Am Soc Nephrol. 1998 May;9(5):903-16
[
9596091.001
]
[Cites]
Genes Dev. 2002 Jun 15;16(12 ):1472-87
[
12080086.001
]
[Cites]
Am J Kidney Dis. 2000 Mar;35(3):427-32
[
10692268.001
]
[Cites]
Am J Physiol. 1999 Jun;276(6 Pt 2):F837-46
[
10362772.001
]
[Cites]
EMBO J. 2004 Apr 7;23(7):1657-68
[
15029248.001
]
[Cites]
N Engl J Med. 1990 Oct 18;323(16):1091-6
[
2215576.001
]
[Cites]
J Clin Endocrinol Metab. 1987 May;64(5):975-9
[
2881944.001
]
[Cites]
N Engl J Med. 1983 Dec 15;309(24):1495-501
[
6139753.001
]
[Cites]
Exp Toxicol Pathol. 2001 Jun;53(2-3):123-8
[
11484829.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Oct 24;97(22):11960-5
[
11035810.001
]
[Cites]
Br Med J (Clin Res Ed). 1986 Jun 28;292(6537):1701-2
[
2873863.001
]
[Cites]
Kidney Int. 1995 Feb;47(2):490-9
[
7723235.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3700-4
[
8170972.001
]
[Cites]
Mol Cell. 2001 Apr;7(4):823-32
[
11336705.001
]
[Cites]
Nat Genet. 2005 Jan;37(1):19-24
[
15624019.001
]
[Cites]
J Biol Chem. 2003 Jan 31;278(5):2807-18
[
12429740.001
]
[Cites]
Cell. 2000 Jul 7;102(1):1-4
[
10929706.001
]
[Cites]
Nat Med. 1997 Oct;3(10):1089-95
[
9334719.001
]
[Cites]
J Biol Chem. 2004 Jan 23;279(4):2975-83
[
14593099.001
]
[Cites]
J Clin Invest. 2001 May;107(9):1145-52
[
11342578.001
]
[Cites]
Physiol Rev. 1997 Jan;77(1):75-197
[
9016301.001
]
[Cites]
J Am Soc Nephrol. 1998 Jul;9(7):1169-77
[
9644626.001
]
[Cites]
Kidney Int. 2000 Jan;57(1):33-40
[
10620185.001
]
[Cites]
Physiol Res. 2004;53(6):629-34
[
15588131.001
]
[Cites]
Nature. 1995 Dec 21-28;378(6559):785-9
[
8524413.001
]
[Cites]
J Hypertens. 1997 Sep;15(9):925-33
[
9321739.001
]
[Cites]
Cell Calcium. 2005 Jun;37(6):593-601
[
15862350.001
]
[Cites]
Science. 2002 Aug 23;297(5585):1352-4
[
12193789.001
]
[Cites]
Oncogene. 1996 Sep 19;13(6):1153-60
[
8808689.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9666-70
[
11493700.001
]
[Cites]
Kidney Int. 1992 May;41(5):1222-36
[
1319521.001
]
[Cites]
Clin Nephrol. 1975;3(3):99-105
[
1139805.001
]
[Cites]
Biochim Biophys Acta. 1999 May 31;1423(3):C19-30
[
10382537.001
]
[Cites]
Contrib Nephrol. 1995;115:118-21
[
8585897.001
]
[Cites]
Kidney Int. 1972 Aug;2(2):107-13
[
4671535.001
]
[Cites]
Transplantation. 2002 Oct 27;74(8):1070-6
[
12438948.001
]
[Cites]
Cell. 2000 Oct 13;103(2):253-62
[
11057898.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3934-9
[
10097141.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 May 10;102(19):6954-9
[
15863619.001
]
[Cites]
Am J Nephrol. 1998;18(5):391-8
[
9730562.001
]
[Cites]
Mol Cell. 2000 Nov;6(5):1267-73
[
11106764.001
]
[Cites]
Biol Cell. 2001 Sep;93(1-2):53-62
[
11730323.001
]
[Cites]
J Am Soc Nephrol. 2000 Aug;11(8):1505-11
[
10906164.001
]
[Cites]
J Urol. 1969 Aug;102(2):156-61
[
5796888.001
]
[Cites]
J Natl Cancer Inst. 1998 Jul 15;90(14):1087-94
[
9672257.001
]
[Cites]
J Am Soc Nephrol. 1995 Jun;5(12):2048-56
[
7579053.001
]
[Cites]
Kidney Int. 2003 Jun;63(6):1983-94
[
12753285.001
]
[Cites]
Pediatr Nephrol. 1988 Jul;2(3):296-302
[
3153029.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Jan 30;98(3):1182-7
[
11252306.001
]
[Cites]
J Clin Endocrinol Metab. 1993 Nov;77(5):1323-8
[
7915721.001
]
[Cites]
Cell. 2003 Jul 11;114(1):61-73
[
12859898.001
]
[Cites]
J Am Soc Nephrol. 2002 Jul;13(7):1733-9
[
12089368.001
]
[Cites]
Nat Cell Biol. 2002 Mar;4(3):191-7
[
11854751.001
]
[Cites]
Nat Med. 2003 Oct;9(10):1323-6
[
14502283.001
]
[Cites]
Kidney Blood Press Res. 2006;29(3):182-8
[
16943682.001
]
[Cites]
Am J Pathol. 1993 Apr;142(4):1051-60
[
8097368.001
]
[Cites]
Kidney Int. 2003 Nov;64(5):1573-9
[
14531789.001
]
[Cites]
Mol Cell Biol. 1998 Nov;18(11):6666-78
[
9774681.001
]
[Cites]
J Urol. 1995 Mar;153(3 Pt 1):578-83
[
7861486.001
]
[Cites]
Kidney Int. 2004 Nov;66(5):1766-73
[
15496147.001
]
[Cites]
Am J Nephrol. 2001 Mar-Apr;21(2):98-103
[
11359016.001
]
[Cites]
JAMA. 1991 Feb 20;265(7):888-92
[
1992187.001
]
[Cites]
J Biol Chem. 1995 Jan 20;270(3):1149-55
[
7836373.001
]
[Cites]
Nephrol Dial Transplant. 1999 May;14(5):1113-6
[
10344347.001
]
[Cites]
Am J Pathol. 2004 Nov;165(5):1719-30
[
15509540.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Apr 4;103(14):5466-71
[
16567633.001
]
[Cites]
Acta Med Scand. 1986;219(4):399-405
[
3716882.001
]
[Cites]
Arch Dermatol Res. 2004 Jul;296(2):74-82
[
15278365.001
]
[Cites]
Curr Opin Pharmacol. 2003 Aug;3(4):371-7
[
12901945.001
]
[Cites]
Cancer Res. 2002 Oct 15;62(20):5645-50
[
12384518.001
]
[Cites]
N Engl J Med. 1995 Jul 6;333(1):18-25
[
7776989.001
]
[Cites]
Kidney Int. 1996 Jan;49(1):135-46
[
8770959.001
]
(PMID = 18034588.001).
[ISSN]
0012-6667
[Journal-full-title]
Drugs
[ISO-abbreviation]
Drugs
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / U01 DK624
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
New Zealand
[Number-of-references]
190
49.
Longenecker CT, Scherzer R, Bacchetti P, Lewis CE, Grunfeld C, Shlipak MG:
HIV viremia and changes in kidney function.
AIDS
; 2009 Jun 1;23(9):1089-96
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[Title]
HIV viremia and changes in
kidney
function.
OBJECTIVE: To evaluate the effect of HIV infection on longitudinal changes in
kidney
function and to identify independent predictors
of kidney
function changes in HIV-infected individuals.
CONCLUSION: Compared with controls, HIV-infected persons were more likely both to have clinical decline and clinical improvement in
kidney
function during 5 years of follow-up.
The extent of viremic control had a strong association with longitudinal changes in
kidney
function.
Genetic Alliance.
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consumer health - HIV/AIDS
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consumer health - HIV/AIDS in Women
.
MedlinePlus Health Information.
consumer health - Kidney Diseases
.
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[Cites]
J Am Soc Nephrol. 2006 Jan;17(1):254-61
[
16267155.001
]
[Cites]
J Am Soc Nephrol. 2005 May;16(5):1404-12
[
15788478.001
]
[Cites]
Antivir Ther. 2006;11(5):641-5
[
16964834.001
]
[Cites]
N Engl J Med. 2006 Nov 30;355(22):2283-96
[
17135583.001
]
[Cites]
AIDS. 2007 May 11;21(8):1003-9
[
17457094.001
]
[Cites]
AIDS. 2007 May 31;21(9):1119-27
[
17502722.001
]
[Cites]
Clin J Am Soc Nephrol. 2006 Jan;1(1):117-29
[
17699198.001
]
[Cites]
Nephrol Dial Transplant. 2007 Nov;22(11):3186-90
[
17575315.001
]
[Cites]
Arch Intern Med. 2007 Nov 12;167(20):2213-9
[
17998494.001
]
[Cites]
Kidney Int. 2007 Dec;72(11):1380-7
[
17805235.001
]
[Cites]
AIDS. 2007 Nov 30;21(18):2435-43
[
18025880.001
]
[Cites]
J Clin Endocrinol Metab. 2008 Jan;93(1):216-24
[
17940113.001
]
[Cites]
Am J Med Sci. 2008 Feb;335(2):89-94
[
18277114.001
]
[Cites]
Am J Kidney Dis. 2008 Mar;51(3):395-406
[
18295055.001
]
[Cites]
AIDS. 2008 Feb 19;22(4):481-7
[
18301060.001
]
[Cites]
Clin Infect Dis. 2008 Apr 15;46(8):1271-81
[
18444867.001
]
[Cites]
Am J Kidney Dis. 2008 Jun;51(6):914-24
[
18455851.001
]
[Cites]
Arch Intern Med. 2008 Nov 10;168(20):2212-8
[
19001197.001
]
[Cites]
AIDS. 2009 Jan 2;23(1):71-82
[
19050388.001
]
[Cites]
Kidney Int. 2009 Feb;75(4):428-34
[
19052538.001
]
[Cites]
Am J Nephrol. 2009;30(3):171-8
[
19349699.001
]
[Cites]
Biometrics. 2000 Sep;56(3):779-88
[
10985216.001
]
[Cites]
Am J Kidney Dis. 2002 Aug;40(2):221-6
[
12148093.001
]
[Cites]
J Am Soc Nephrol. 2002 Dec;13(12):2997-3004
[
12444220.001
]
[Cites]
AIDS. 2004 Feb 20;18(3):541-6
[
15090808.001
]
[Cites]
Kidney Int. 2004 Sep;66(3):1145-52
[
15327410.001
]
[Cites]
J Clin Epidemiol. 1988;41(11):1105-16
[
3204420.001
]
[Cites]
Am J Nephrol. 1995;15(3):217-21
[
7618646.001
]
[Cites]
Kidney Int. 1995 Aug;48(2):311-20
[
7564098.001
]
[Cites]
Scand J Clin Lab Invest. 1999 Feb;59(1):1-8
[
10206092.001
]
[Cites]
Stat Methods Med Res. 1999 Mar;8(1):3-15
[
10347857.001
]
[Cites]
J Am Soc Nephrol. 2004 Dec;15(12):3184-91
[
15579522.001
]
[Cites]
J Am Soc Nephrol. 2005 Feb;16(2):459-66
[
15615823.001
]
[Cites]
Am J Epidemiol. 2006 May 1;163(9):860-9
[
16524955.001
]
(PMID = 19352136.001).
[ISSN]
1473-5571
[Journal-full-title]
AIDS (London, England)
[ISO-abbreviation]
AIDS
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / R01-HL-74814; United States / NIDDK NIH HHS / DK / R01 DK057508-01S1; United States / NCRR NIH HHS / RR / M01 RR000083-38S30468; United States / NIDDK NIH HHS / DK / R01 DK057508; United States / NCRR NIH HHS / RR / M01-RR00083; United States / NHLBI NIH HHS / HL / R01 HL074814-07; United States / NIDDK NIH HHS / DK / R01 DK057508-01; United States / NCRR NIH HHS / RR / M01 RR000083-380468; United States / NCRR NIH HHS / RR / M01 RR000083-40S10468; United States / NCRR NIH HHS / RR / M01 RR000083-430512; United States / NCRR NIH HHS / RR / M01 RR000865; United States / NCRR NIH HHS / RR / M01 RR000036; United States / NHLBI NIH HHS / HL / R01 HL074814-04; United States / NCRR NIH HHS / RR / M01 RR000083-38S20468; United States / NCRR NIH HHS / RR / M01 RR000083-420512; United States / NHLBI NIH HHS / HL / R01 HL074814-06; United States / NIDDK NIH HHS / DK / R01 DK057508-03S1; United States / NCRR NIH HHS / RR / M01 RR000054; United States / NCRR NIH HHS / RR / M01-RR00052; United States / NIDDK NIH HHS / DK / R01 DK057508-03S2; United States / NCRR NIH HHS / RR / M01 RR000052; United States / NHLBI NIH HHS / HL / R01 HL074814-05; United States / NCRR NIH HHS / RR / M01 RR000051; United States / NCRR NIH HHS / RR / M01-RR00051; United States / NCRR NIH HHS / RR / M01-RR00036; United States / NHLBI NIH HHS / HL / R01 HL074814; United States / NIDDK NIH HHS / DK / R01 DK057508-02; United States / NCRR NIH HHS / RR / M01 RR000083-400468; United States / NHLBI NIH HHS / HL / R01-HL-53359; United States / NCRR NIH HHS / RR / M01-RR00636; United States / NCRR NIH HHS / RR / M01 RR000083-390468; United States / NCRR NIH HHS / RR / M01-RR00054; United States / NCRR NIH HHS / RR / M01 RR000083; United States / NIDDK NIH HHS / DK / R01 DK057508-03; United States / NIDDK NIH HHS / DK / R01-DK-57508
[Publication-type]
Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cystatin C
[Other-IDs]
NLM/ NIHMS492632; NLM/ PMC3725756
50.
Goldstein SL, Devarajan P:
Progression from acute kidney injury to chronic kidney disease: a pediatric perspective.
Adv Chronic Kidney Dis
; 2008 Jul;15(3):278-83
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[Title]
Progression from acute
kidney
injury to chronic
kidney
disease: a pediatric perspective.
Although emerging evidence indicates that the incidence of both acute
kidney
injury (AKI) and chronic
kidney
disease (CKD) in children is rising and the etiologies are dramatically changing, relatively little is currently known regarding the potential for transition from AKI to CKD.
These include neutrophil gelatinase-associated lipocalin, liver-type fatty acid-binding protein, and
kidney
injury molecule-1.
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[Cites]
Nephrol Dial Transplant. 2008 Jan;23(1):414-6
[
17893105.001
]
[Cites]
Transplantation. 2007 Dec 27;84(12):1625-30
[
18165774.001
]
[Cites]
Kidney Int. 2008 Feb;73(4):465-72
[
18094680.001
]
[Cites]
Curr Opin Nephrol Hypertens. 2008 Mar;17(2):127-32
[
18277143.001
]
[Cites]
Crit Care. 2007;11(6):R127
[
18070344.001
]
[Cites]
Clin J Am Soc Nephrol. 2008 May;3(3):665-73
[
18337554.001
]
[Cites]
Pediatr Crit Care Med. 2008 May;9(3):279-84
[
18446113.001
]
[Cites]
Adv Chronic Kidney Dis. 2008 Jul;15(3):222-34
[
18565474.001
]
[Cites]
Pediatr Nephrol. 2000 Nov;15(1-2):11-3
[
11095002.001
]
[Cites]
Curr Opin Pediatr. 2002 Apr;14(2):183-8
[
11981288.001
]
[Cites]
Kidney Int. 2002 Jul;62(1):237-44
[
12081583.001
]
[Cites]
Crit Care Med. 2002 Sep;30(9):2156-7
[
12352064.001
]
[Cites]
Pediatr Nephrol. 2002 Dec;17(12):1032-7
[
12478353.001
]
[Cites]
Kidney Int. 2003 May;63(5):1714-24
[
12675847.001
]
[Cites]
Pediatr Nephrol. 2003 Aug;18(8):796-804
[
12811650.001
]
[Cites]
J Am Soc Nephrol. 2003 Oct;14(10):2534-43
[
14514731.001
]
[Cites]
Ann Thorac Surg. 2003 Nov;76(5):1443-9
[
14602265.001
]
[Cites]
Pediatr Nephrol. 2004 Jan;19(1):91-5
[
14634863.001
]
[Cites]
Am J Nephrol. 2004 May-Jun;24(3):307-15
[
15148457.001
]
[Cites]
Crit Care. 2004 Aug;8(4):R204-12
[
15312219.001
]
[Cites]
Am J Kidney Dis. 1995 Jan;25(1):113-8
[
7810517.001
]
[Cites]
Am J Kidney Dis. 2005 Jan;45(1):96-101
[
15696448.001
]
[Cites]
Lancet. 2005 Apr 2-8;365(9466):1231-8
[
15811456.001
]
[Cites]
J Am Soc Nephrol. 2005 Nov;16(11):3365-70
[
16177006.001
]
[Cites]
Am J Kidney Dis. 2005 Dec;46(6):1038-48
[
16310569.001
]
[Cites]
J Am Soc Nephrol. 2005 Dec;16(12):3736-41
[
16267160.001
]
[Cites]
Kidney Int. 2006 Jan;69(1):184-9
[
16374442.001
]
[Cites]
Ann Thorac Surg. 2006 Feb;81(2):542-6
[
16427848.001
]
[Cites]
Mol Cell Biochem. 2006 Mar;284(1-2):175-82
[
16532260.001
]
[Cites]
Pediatr Nephrol. 2006 Jun;21(6):856-63
[
16528543.001
]
[Cites]
Pediatr Nephrol. 2006 Jul;21(7):989-94
[
16773412.001
]
[Cites]
Crit Care Med. 2006 Jul;34(7):1913-7
[
16715038.001
]
[Cites]
Am J Transplant. 2006 Jul;6(7):1639-45
[
16827865.001
]
[Cites]
Crit Care. 2006;10(3):R73
[
16696865.001
]
[Cites]
Arthritis Rheum. 2006 Aug;54(8):2577-84
[
16868980.001
]
[Cites]
Pediatrics. 2006 Sep;118(3):e786-91
[
16894011.001
]
[Cites]
Pediatr Nephrol. 2007 Jan;22(1):101-8
[
17072653.001
]
[Cites]
Pediatr Crit Care Med. 2007 Jan;8(1):29-35
[
17251879.001
]
[Cites]
Clin Immunol. 2007 May;123(2):227-34
[
17360238.001
]
[Cites]
Kidney Int. 2007 May;71(10):1028-35
[
17396113.001
]
[Cites]
J Pathol. 2007 Jun;212(2):209-17
[
17471468.001
]
[Cites]
Am J Nephrol. 2007;27(4):373-8
[
17570904.001
]
[Cites]
Kidney Int. 2007 Aug;72(3):348-58
[
17495861.001
]
[Cites]
Am J Kidney Dis. 2007 Aug;50(2):169-80
[
17660017.001
]
[Cites]
Clin J Am Soc Nephrol. 2006 Sep;1(5):1006-15
[
17699320.001
]
[Cites]
J Am Soc Nephrol. 2007 Oct;18(10):2704-14
[
17898236.001
]
[Cites]
J Am Soc Nephrol. 2007 Nov;18(11):2894-902
[
17942962.001
]
[Cites]
Pediatr Nephrol. 2007 Dec;22(12):2089-95
[
17874137.001
]
[Cites]
Semin Nephrol. 2007 Nov;27(6):637-51
[
18061846.001
]
[Cites]
Crit Care. 2007;11(4):R84
[
17678545.001
]
(PMID = 18565478.001).
[ISSN]
1548-5609
[Journal-full-title]
Advances in chronic kidney disease
[ISO-abbreviation]
Adv Chronic Kidney Dis
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK069749-04; United States / NIDDK NIH HHS / DK / DK069749-04; United States / NIDDK NIH HHS / DK / R21 DK070163-02; United States / NIDDK NIH HHS / DK / R01 DK069749; United States / NIDDK NIH HHS / DK / R21 DK070163
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers
[Number-of-references]
54
[Other-IDs]
NLM/ NIHMS57871; NLM/ PMC2481383
51.
Doctor RB, Serkova NJ, Hasebroock KM, Zafar I, Edelstein CL:
Distinct patterns of kidney and liver cyst growth in pkd2(WS25/-) mice.
Nephrol Dial Transplant
; 2010 Nov;25(11):3496-504
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[Title]
Distinct patterns
of kidney
and liver cyst growth in pkd2(WS25/-) mice.
BACKGROUND: Autosomal dominant polycystic
kidney
disease (ADPKD) is a common genetic disease that results in the development of cystic
kidneys
and liver.
Providing the foundation for future long-term studies, the present work documents distinct patterns of long-term cyst growth in
the kidneys
and liver of male and female pkd2(WS25/-) mice.
METHODS: Gravimetric measurements documented the progression
of kidney
and liver growth in male and female pkd2(WS25/-) mice over 12 months.
A fast imaging with steady-state precision-magnetic resonance imaging (FISP-MRI) technique to measure
kidney
and liver organ and cyst volumes was optimized and validated.
RESULTS: Male and female pkd2(WS25/-) mice had significant increases in
kidney
weights after 4 months of age.
The progression
of kidney
growth was minimal after 4 months of age.
CONCLUSIONS: Pkd2(WS25/-) mice are a genetic mouse model that recapitulates the early phenotypic characteristics of human ADPKD
kidney
cystogenesis.
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[Cites]
Hepatology. 1988 Nov-Dec;8(6):1627-34
[
3192176.001
]
[Cites]
Kidney Int. 2004 Apr;65(4):1511-6
[
15086495.001
]
[Cites]
Magn Reson Imaging. 1991;9(3):429-34
[
1881263.001
]
[Cites]
Hepatology. 1997 Nov;26(5):1282-6
[
9362373.001
]
[Cites]
Cell. 1998 Apr 17;93(2):177-88
[
9568711.001
]
[Cites]
N Engl J Med. 2006 May 18;354(20):2122-30
[
16707749.001
]
[Cites]
Nephron Clin Pract. 2006;103(4):c173-80
[
16636585.001
]
[Cites]
J Magn Reson Imaging. 2006 Sep;24(3):646-56
[
16878308.001
]
[Cites]
N Engl J Med. 2007 Apr 12;356(15):1560
[
17429087.001
]
[Cites]
Clin J Am Soc Nephrol. 2006 Jan;1(1):64-9
[
17699192.001
]
[Cites]
Clin Cancer Res. 2007 Nov 1;13(21):6450-8
[
17975157.001
]
[Cites]
Kidney Int. 2008 Mar;73(6):778-81
[
18185504.001
]
[Cites]
Am J Physiol Lung Cell Mol Physiol. 2008 Jul;295(1):L152-61
[
18441091.001
]
[Cites]
AJR Am J Roentgenol. 2008 Aug;191(2):352-8
[
18647901.001
]
[Cites]
N Engl J Med. 2008 Oct 2;359(14):1477-85
[
18832246.001
]
[Cites]
Acad Radiol. 2009 Jan;16(1):88-95
[
19064216.001
]
[Cites]
Kidney Int. 2009 Jan;75(2):235-41
[
18971924.001
]
[Cites]
J Am Soc Nephrol. 2009 Jan;20(1):6-8
[
19073819.001
]
[Cites]
Recent Pat Anticancer Drug Discov. 2009 Jan;4(1):36-53
[
19149687.001
]
[Cites]
Annu Rev Med. 2009;60:321-37
[
18947299.001
]
[Cites]
Nat Genet. 2000 Jan;24(1):75-8
[
10615132.001
]
[Cites]
J Am Soc Nephrol. 2000 Aug;11(8):1505-11
[
10906164.001
]
[Cites]
Kidney Int. 2000 Dec;58(6):2492-501
[
11115083.001
]
[Cites]
Comp Med. 2002 Oct;52(5):433-8
[
12405636.001
]
[Cites]
J Magn Reson Imaging. 2003 Feb;17(2):190-6
[
12541226.001
]
[Cites]
Kidney Int. 2003 Sep;64(3):1035-45
[
12911554.001
]
[Cites]
Hepatology. 1990 Jun;11(6):1033-7
[
2365280.001
]
(PMID = 20388629.001).
[ISSN]
1460-2385
[Journal-full-title]
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
[ISO-abbreviation]
Nephrol. Dial. Transplant.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK-074835; United States / NCRR NIH HHS / RR / UL1 RR025780; United States / NIDDK NIH HHS / DK / R01 DK074835; United States / NCI NIH HHS / CA / P30 CA046934; United States / NIDDK NIH HHS / DK / DK-056851; United States / NIDDK NIH HHS / DK / R01 DK056851
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / TRPP Cation Channels; 0 / polycystic kidney disease 2 protein
[Other-IDs]
NLM/ PMC2980992
52.
Collan Y, Hirsimäki P, Aho H, Wuorela M, Sundström J, Tertti R, Metsärinne K:
Value of electron microscopy in kidney biopsy diagnosis.
Ultrastruct Pathol
; 2005 Nov-Dec;29(6):461-8
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[Title]
Value of electron microscopy in
kidney
biopsy
diagnosis
.
Kidney
biopsy reports given during 2003 were collected from the authors' pathology database.
Five
tumor
samples were not studied with electron microscopy (EM).
EM was not performed in 10/24 transplant biopsies, or in 11/82 cases of suspected primary
kidney
disease.
(1) EM was essential for
diagnosis
, (2) EM contributed to the interpretation and cleared uncertainties, and (3) EM had no influence on the diagnostic process.
In transplant biopsies EM influenced the final
diagnosis
in 86% of cases (category 2).
In biopsies performed for primary
kidney
disease EM was essential for
diagnosis
in 18.3% clearly contributed in 53.5%, and had no influence on the final
diagnosis
in 28.2% of cases.
Because only about 25% of the EM reports did not have any influence on the diagnostic process, it is recommended that
kidney
biopsy protocols should include EM in all biopsy cases, or at least tissue should be reserved for EM studies of all cases.
[MeSH-major]
Kidney
/ ultrastructure.
Kidney
Diseases /
diagnosis
[MeSH-minor]
Adult. Aged. Biopsy.
Diagnosis
, Differential. Humans.
Kidney
Transplantation / pathology. Male. Microscopy, Electron, Transmission
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(PMID = 16316946.001).
[ISSN]
0191-3123
[Journal-full-title]
Ultrastructural pathology
[ISO-abbreviation]
Ultrastruct Pathol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
53.
Rodrigo E, Arias M:
A practical approach to immune monitoring in kidney transplantation.
Minerva Urol Nefrol
; 2007 Sep;59(3):337-52
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[Title]
A practical approach to immune monitoring in
kidney
transplantation.
In the last years, there has been a growing interest in the development of new assays available to monitor
kidney
transplantation.
These assays will permit strategies for the minimization of immunosuppression, for induction of operational tolerance, for an early and noninvasive
diagnosis of
acute rejection, for prevention of adverse effects of immunosuppressive drugs and for measurement of the net immunosuppressive state.
Today, there is not one test that helps us monitor the outcome
of kidney
recipients safely.
Further studies and further developed assays are needed to obtain an adequate immune monitoring strategy in
kidney
transplantation.
Transvivo DTH assay, tetramer staining, quantification of cell proliferation by CFSE labelling, human leukocyte antigen-G determination, phenotyping of recipient immune cells, detection of tolerogeneic dendritic cell precursors, T-cell receptor landscaping and quantification of gene and protein expression need more studies to know their exact role as monitoring markers in
kidney
transplant patients.
[MeSH-major]
Kidney
Transplantation / immunology. Monitoring, Immunologic
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(PMID = 17912229.001).
[ISSN]
0393-2249
[Journal-full-title]
Minerva urologica e nefrologica = The Italian journal of urology and nephrology
[ISO-abbreviation]
Minerva Urol Nefrol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Italy
[Number-of-references]
96
54.
Feyssa E, Jones-Burton C, Ellison G, Philosophe B, Howell C:
Racial/ethnic disparity in kidney transplantation outcomes: influence of donor and recipient characteristics.
J Natl Med Assoc
; 2009 Feb;101(2):111-5
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[Title]
Racial/ethnic disparity in
kidney
transplantation outcomes: influence of donor and recipient characteristics.
OBJECTIVE: The purpose of this study was to evaluate the basis for the racial/ethnic disparity in
kidney
allograft survival.
METHODS: We conducted a retrospective study of 2130 patients who underwent
kidney
transplantation between January 1995 and December 2003.
Additionally, black recipients were more likely to have a prior
kidney
transplant (16.7% vs 11.0%) and to have a cadaver
kidney
donor (74% vs 56.5%).
Previous
kidney
transplantation, cadaveric donor, donor age, recipient employment status, and recipient tobacco use were associated with allograft survival in a Cox proportional hazard model.
CONCLUSIONS: Graft survival rate in black
kidney
transplant recipients is significantly lower than whites, and this disparity can be partially explained by the low rate of live donors and a higher previous transplantation rate in blacks.
[MeSH-major]
Graft Survival. Healthcare Disparities / statistics & numerical data.
Kidney
Transplantation / ethnology.
Kidney
Transplantation / immunology
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.
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(PMID = 19378626.001).
[ISSN]
1943-4693
[Journal-full-title]
Journal of the National Medical Association
[ISO-abbreviation]
J Natl Med Assoc
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
55.
Hirsch S:
Prerenal success in chronic kidney disease.
Am J Med
; 2007 Sep;120(9):754-9
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[Title]
Prerenal success in chronic
kidney
disease.
Renin-angiotensin system inhibitors and diuretics are commonly prescribed to patients with chronic
kidney
disease to reduce systemic blood pressure.
Several reasons for this reluctance are discussed, including the failure to distinguish between hemodynamic- and parenchymal-mediated changes in
kidney
function.
Finally, recent literature describing harmful effects of increases in serum creatinine in other cohorts is reviewed; these cohorts are sufficiently different from the stable chronic
kidney
disease patient that the results ought not to be extrapolated.
[MeSH-major]
Renal
Insufficiency, Chronic / physiopathology
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(PMID = 17765040.001).
[ISSN]
1555-7162
[Journal-full-title]
The American journal of medicine
[ISO-abbreviation]
Am. J. Med.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
AYI8EX34EU / Creatinine
[Number-of-references]
36
56.
Gheith OA, El-Saadany SA, Abuo Donia SA, Salem YM:
Compliance of kidney transplant patients to the recommended lifestyle behaviours: single centre experience.
Int J Nurs Pract
; 2008 Oct;14(5):398-407
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[Title]
Compliance
of kidney
transplant patients to the recommended lifestyle behaviours: single centre experience.
Successful management
of kidney
transplant patients requires lifelong therapeutic regimen.
The aim of the study was to identify compliance
of kidney
transplant patients to the recommended lifestyle behaviours.
One hundred adult
kidney
transplant patients of 6 months duration and more participated in this study regardless of age or sex.
A structured questionnaire was developed which included socio-demographic characteristics, the recommended lifestyle behaviours of the
kidney
transplant patients and
the kidney
transplant patient's health condition and his results from the laboratory tests.
The nurse must provide
the kidney
transplant patients with the necessary knowledge of the recommended lifestyle behaviours.
[MeSH-major]
Kidney
Transplantation. Life Style. Patient Compliance
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(PMID = 18808541.001).
[ISSN]
1440-172X
[Journal-full-title]
International journal of nursing practice
[ISO-abbreviation]
Int J Nurs Pract
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Australia
[Chemical-registry-number]
0 / Immunosuppressive Agents
57.
Briet M, Schiffrin EL:
Aldosterone: effects on the kidney and cardiovascular system.
Nat Rev Nephrol
; 2010 May;6(5):261-73
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[Title]
Aldosterone: effects on
the kidney
and cardiovascular system.
Aldosterone, a steroid hormone with mineralocorticoid activity, is mainly recognized for its action on sodium reabsorption in the distal nephron of the
kidney
, which is mediated by the epithelial sodium channel (ENaC).
Beyond this well-known action, however, aldosterone exerts other effects on
the kidney
, blood vessels and the heart, which can have pathophysiological consequences, particularly in the presence of a high salt intake.
Aldosterone is implicated in
renal
inflammatory and fibrotic processes, as well as in podocyte injury and mesangial cell proliferation.
Small interventional studies in patients with chronic
kidney
disease have shown promising results, with a significant reduction of proteinuria associated with aldosterone antagonism, but large interventional trials that test the efficacy and safety of mineralocorticoid-receptor antagonists in chronic
kidney
disease are needed.
[MeSH-major]
Aldosterone / adverse effects. Aldosterone / pharmacology. Angiotensin II Type 1 Receptor Blockers / pharmacology. Cardiovascular Diseases / chemically induced. Cardiovascular Diseases / drug therapy. Cardiovascular System / drug effects.
Kidney
/ drug effects. Mineralocorticoid Receptor Antagonists / pharmacology
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(PMID = 20234356.001).
[ISSN]
1759-507X
[Journal-full-title]
Nature reviews. Nephrology
[ISO-abbreviation]
Nat Rev Nephrol
[Language]
eng
[Grant]
Canada / Canadian Institutes of Health Research / / 37917; Canada / Canadian Institutes of Health Research / / 82790
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Angiotensin II Type 1 Receptor Blockers; 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Mineralocorticoid Receptor Antagonists; 0 / Sodium Channels; 0 / Sodium, Dietary; 4964P6T9RB / Aldosterone
[Number-of-references]
141
58.
Ashrith G, Elayda MA, Wilson JM:
Revascularization options in patients with chronic kidney disease.
Tex Heart Inst J
; 2010;37(1):9-18
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[Title]
Revascularization options in patients with chronic
kidney
disease.
Cardiovascular disease is the leading cause of death in patients who have chronic
kidney
disease or end-stage
renal
disease and are undergoing hemodialysis.
Chronic
kidney
disease is a recognized risk factor for premature atherosclerosis.
Unfortunately, most major randomized clinical trials that form the basis for evidence-based use of revascularization procedures exclude patients who have
renal
insufficiency.
Retrospective, observational studies suggest that patients with end-stage
renal
disease and severe coronary occlusive disease have a lower risk of death if they undergo coronary revascularization rather than medical therapy alone.
This difference appears to result from poor long-term results of percutaneous coronary intervention in patients who have chronic
kidney
disease or end-stage
renal
disease.Because randomized trials comparing percutaneous coronary intervention and coronary artery bypass grafting have included patients undergoing balloon angioplasty and placement of bare-metal stents, their conclusions are suspect in the era of drug-eluting stents.
In this review, we discuss different revascularization options for patients with chronic
kidney
disease, the outcomes of revascularization procedures, and the risk factors for adverse outcomes.
Genetic Alliance.
consumer health - Kidney Disease
.
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[Cites]
Chest. 2005 Aug;128(2):855-62
[
16100178.001
]
[Cites]
J Thorac Cardiovasc Surg. 2005 Sep;130(3):746-52
[
16153923.001
]
[Cites]
Circulation. 2005 Aug 30;112(9 Suppl):I270-5
[
16159830.001
]
[Cites]
J Interv Cardiol. 2005 Oct;18(5):331-7
[
16202107.001
]
[Cites]
Ann Thorac Surg. 2005 Dec;80(6):2148-53
[
16305860.001
]
[Cites]
Am Heart J. 2005 Dec;150(6):1163-70
[
16338253.001
]
[Cites]
Ann Thorac Surg. 2006 Feb;81(2):591-8; discussion 598
[
16427858.001
]
[Cites]
Circulation. 2006 Feb 28;113(8):1063-70
[
16490821.001
]
[Cites]
Kidney Blood Press Res. 2005;28(5-6):270-4
[
16534220.001
]
[Cites]
Eur J Cardiothorac Surg. 2006 Apr;29(4):461-5
[
16483789.001
]
[Cites]
J Am Soc Nephrol. 2006 Apr;17(4):1175-80
[
16481413.001
]
[Cites]
J Thorac Cardiovasc Surg. 2006 Jun;131(6):1261-6
[
16733155.001
]
[Cites]
J Invasive Cardiol. 2006 Jun;18(6):273-7
[
16751681.001
]
[Cites]
Kidney Int. 2006 Aug;70(4):757-64
[
16788687.001
]
[Cites]
J Invasive Cardiol. 2006 Sep;18(9):405-8
[
16954577.001
]
[Cites]
J Invasive Cardiol. 2006 Sep;18(9):409-10
[
16954578.001
]
[Cites]
Ann Thorac Cardiovasc Surg. 2006 Aug;12(4):257-64
[
16977295.001
]
[Cites]
J Invasive Cardiol. 2006 Dec;18(12):577-83
[
17197706.001
]
[Cites]
Circulation. 2007 Jul 17;116(3):298-304
[
17606842.001
]
[Cites]
J Invasive Cardiol. 2007 Aug;19(8):331-7
[
17712200.001
]
[Cites]
Clin Transplant. 2007 Sep-Oct;21(5):609-14
[
17845634.001
]
[Cites]
JAMA. 2007 Nov 7;298(17):2038-47
[
17986697.001
]
[Cites]
Am J Kidney Dis. 2008 Jan;51(1 Suppl 1):S1-320
[
18086389.001
]
[Cites]
J Am Coll Cardiol. 2008 May 27;51(21):2017-24
[
18498954.001
]
[Cites]
Ann Thorac Surg. 1999 Oct;68(4):1257-61
[
10543489.001
]
[Cites]
Kidney Int. 2000 Jan;57(1):307-13
[
10620213.001
]
[Cites]
Cardiol Rev. 2008 Jul-Aug;16(4):213-8
[
18562812.001
]
[Cites]
Circulation. 2008 Oct 28;118(18):1817-27
[
18852368.001
]
[Cites]
Circulation. 2008 Nov 18;118(21):2130-8
[
18981306.001
]
[Cites]
Artif Organs. 2001 Apr;25(4):239-47
[
11318749.001
]
[Cites]
Artif Organs. 2001 Apr;25(4):268-72
[
11318755.001
]
[Cites]
Ital Heart J. 2001 May;2(5):379-83
[
11392643.001
]
[Cites]
Kidney Int. 2001 Jul;60(1):292-9
[
11422764.001
]
[Cites]
Jpn J Thorac Cardiovasc Surg. 2001 Nov;49(11):660-5
[
11757338.001
]
[Cites]
Circulation. 2004 Jun 15;109(23):2866-71
[
15159290.001
]
[Cites]
Eur J Cardiothorac Surg. 1999 Jan;15(1):51-4
[
10077373.001
]
[Cites]
Artif Organs. 2003 Feb;27(2):174-80
[
12580775.001
]
[Cites]
Am J Cardiol. 2000 Jun 1;85(11):1365-8
[
10831956.001
]
[Cites]
Am J Cardiol. 2000 Aug 15;86(4):395-9
[
10946031.001
]
[Cites]
Am J Cardiol. 2000 Sep 1;86(5):485-9
[
11009262.001
]
[Cites]
Ann Thorac Surg. 2000 Sep;70(3):813-8; discussion 819
[
11016315.001
]
[Cites]
Circulation. 2000 Dec 12;102(24):2973-7
[
11113048.001
]
[Cites]
Ann Thorac Surg. 2001 Feb;71(2):543-8
[
11235703.001
]
[Cites]
Heart. 2001 May;85(5):556-60
[
11303010.001
]
[Cites]
Am J Nephrol. 1999;19(1):38-44
[
10085448.001
]
[Cites]
Eur J Cardiothorac Surg. 1999 May;15(5):691-6
[
10386419.001
]
[Cites]
Kidney Int. 1999 Jul;56(1):324-32
[
10411709.001
]
[Cites]
Ann Thorac Surg. 2004 Dec;78(6):2044-9
[
15561032.001
]
[Cites]
Am J Cardiol. 2005 Jan 15;95(2):167-72
[
15642546.001
]
[Cites]
Scand J Urol Nephrol. 2004;38(5):405-16
[
15764253.001
]
[Cites]
Ann Thorac Surg. 2005 May;79(5):1577-83
[
15854936.001
]
[Cites]
Circulation. 2005 May 31;111(21):2858-64
[
15927994.001
]
[Cites]
Eur Heart J. 2005 Aug;26(15):1488-93
[
15860519.001
]
[Cites]
Jpn J Thorac Cardiovasc Surg. 2001 Dec;49(12):693-9
[
11808090.001
]
[Cites]
J Am Coll Cardiol. 2002 Apr 3;39(7):1113-9
[
11923033.001
]
[Cites]
Int Urol Nephrol. 2001;32(4):717-23
[
11989572.001
]
[Cites]
Circulation. 2002 May 14;105(19):2253-8
[
12010906.001
]
[Cites]
Circulation. 2002 Oct 22;106(17):2207-11
[
12390949.001
]
[Cites]
Ann Thorac Surg. 2003 Feb;75(2):496-500
[
12607660.001
]
[Cites]
Kidney Int. 2003 Mar;63(3):1121-9
[
12631096.001
]
[Cites]
Circulation. 2003 Jun 3;107(21):2653-5
[
12756161.001
]
[Cites]
J Am Soc Nephrol. 2003 Sep;14(9):2373-80
[
12937316.001
]
[Cites]
Am J Cardiol. 2003 Sep 15;92(6):721-5
[
12972118.001
]
[Cites]
J Am Soc Nephrol. 2003 Oct;14(10):2556-72
[
14514733.001
]
[Cites]
J Am Soc Nephrol. 2004 Mar;15(3):517-23
[
14978153.001
]
[Cites]
Kidney Int. 2004 Jul;66(1):441-7
[
15200454.001
]
[Cites]
Am J Cardiol. 2004 Jul 1;94(1):30-4
[
15219504.001
]
[Cites]
Am J Kidney Dis. 2004 Oct;44(4):627-35
[
15384013.001
]
[Cites]
J Card Surg. 2004 Sep-Oct;19(5):449-52
[
15383059.001
]
[Cites]
Am Heart J. 2004 Sep;148(3):430-8
[
15389229.001
]
[Cites]
Mayo Clin Proc. 1991 Jan;66(1):45-53
[
1988758.001
]
[Cites]
Am J Kidney Dis. 1995 Feb;25(2):281-90
[
7847356.001
]
[Cites]
Ann Thorac Surg. 1996 Jun;61(6):1793-6
[
8651786.001
]
[Cites]
N Engl J Med. 1996 Jul 25;335(4):217-25
[
8657237.001
]
[Cites]
Heart. 1997 Oct;78(4):337-42
[
9404246.001
]
[Cites]
Cardiovasc Surg. 1998 Oct;6(5):500-5
[
9794271.001
]
(PMID = 20200622.001).
[ISSN]
1526-6702
[Journal-full-title]
Texas Heart Institute journal
[ISO-abbreviation]
Tex Heart Inst J
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
76
[Other-IDs]
NLM/ PMC2829816
[Keywords]
NOTNLM ; Angioplasty, transluminal, percutanous coronary / coronary artery bypass / coronary artery bypass, off-pump / creatinine/blood/metabolism / drug-eluting stents / extracorporeal circulation / glomerular filtration rate / kidney failure, chronic / renal dialysis / stents / treatment outcome
59.
Parzanese I, Maccarone D, Caniglia L, Pisani F, Mazzotta C, Rizza V, Famulari A:
Risk factors that can influence kidney transplant outcome.
Transplant Proc
; 2006 May;38(4):1022-3
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[Title]
Risk factors that can influence
kidney
transplant outcome.
The survival and function of a
kidney
transplant are influenced by numerous immunological and nonimmunological factors.
The aim of this study was to evaluate the role of a number of cadaveric donor parameters on transplanted
kidney
function, and in particular on the occurrence of delayed graft function (DGF) since DGF is one of the most important factors in long-term organ survival.
This study looked at 143 patients who underwent
kidney
transplant of whom 32 displayed DGF.
We observed that a donor history of hypertension (46.8% DGF vs 23.27% no DGF; P = .01) and high levels of donor creatinine prior to organ removal (1.9 +/- 1.2 mg/dL DGF vs 1.2 +/- 0.9 mg/dL no DGF; P = .007) were significant risk factors for DGF among
kidney
recipients.
[MeSH-major]
Delayed Graft Function / physiopathology. Graft Survival / physiology.
Kidney
Transplantation / adverse effects.
Kidney
Transplantation / physiology
[MeSH-minor]
Cadaver. Creatinine / blood. Follow-Up Studies. Humans.
Kidney
Function Tests. Retrospective Studies. Risk Factors. Time Factors. Tissue Donors / statistics & numerical data. Treatment Outcome
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(PMID = 16757251.001).
[ISSN]
0041-1345
[Journal-full-title]
Transplantation proceedings
[ISO-abbreviation]
Transplant. Proc.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
AYI8EX34EU / Creatinine
60.
Campese VM, Hadaya B, Chiu J:
HMG-CoA reductase inhibitors and the kidney.
Curr Hypertens Rep
; 2005 Oct;7(5):337-42
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[Title]
HMG-CoA reductase inhibitors and
the kidney
.
It has not been well established whether statins confer similar benefits to
the kidney
.
In this review, we critically consider the available data whereby dyslipidemia mediates
renal
dysfunction by modulating the inflammatory response to diverse cytokines.
We also review the emerging database suggesting that statins may modulate
renal
dysfunction by altering the response of the
kidney
to dyslipidemia, particularly in patients with end-stage
renal
disease (ESRD) and post-
kidney
transplant.
[MeSH-major]
Cardiovascular Diseases / prevention & control. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use.
Kidney
Diseases / therapy
[MeSH-minor]
Dyslipidemias / complications. Dyslipidemias / drug therapy. Humans. Inflammation / drug therapy.
Kidney
Failure, Chronic / complications.
Kidney
Failure, Chronic / therapy.
Kidney
Transplantation
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[Cites]
Transplantation. 1996 May 27;61(10):1469-74
[
8633373.001
]
[Cites]
Arterioscler Thromb Vasc Biol. 2003 Jan 1;23 (1):58-63
[
12524225.001
]
[Cites]
Arterioscler Thromb Vasc Biol. 2002 Sep 1;22(9):1452-8
[
12231565.001
]
[Cites]
Arterioscler Thromb Vasc Biol. 2003 May 1;23(5):729-36
[
12615672.001
]
[Cites]
Circulation. 1997 Mar 4;95(5):1126-31
[
9054840.001
]
[Cites]
J Clin Invest. 1998 Jun 15;101(12):2711-9
[
9637705.001
]
[Cites]
Transplantation. 1994 Jan;57(1):68-72
[
8291116.001
]
[Cites]
Atherosclerosis. 2002 Jan;160(1):141-6
[
11755931.001
]
[Cites]
J Hypertens. 2002 Dec;20(12):2465-73
[
12473872.001
]
[Cites]
BMC Cardiovasc Disord. 2003 Jul 19;3:6
[
12871602.001
]
[Cites]
JAMA. 2004 Mar 3;291(9):1071-80
[
14996776.001
]
[Cites]
Ann Intern Med. 2003 Oct 21;139(8):670-82
[
14568856.001
]
[Cites]
Kidney Int Suppl. 1999 Jul;71:S10-3
[
10412727.001
]
[Cites]
N Engl J Med. 1997 Aug 7;337(6):408-16
[
9241131.001
]
[Cites]
Kidney Int. 1993 Apr;43(4):918-27
[
8479130.001
]
[Cites]
Hypertension. 1995 Oct;26(4):670-5
[
7558229.001
]
[Cites]
N Engl J Med. 2001 Nov 8;345(19):1419-21
[
11794177.001
]
[Cites]
Nephron. 2002 Apr;90(4):373-8
[
11961394.001
]
[Cites]
Kidney Int Suppl. 1999 Jul;71:S84-7
[
10412745.001
]
[Cites]
J Nephrol. 2003 Mar-Apr;16(2):238-44
[
12768071.001
]
[Cites]
J Am Soc Nephrol. 1993 Aug;4(2):187-94
[
8400082.001
]
[Cites]
J Clin Pathol. 2004 Jul;57(7):728-34
[
15220366.001
]
[Cites]
N Engl J Med. 2004 Sep 23;351(13):1285-95
[
15385655.001
]
[Cites]
Transplantation. 2001 Jul 27;72(2):223-7
[
11477342.001
]
[Cites]
Kidney Int. 1993 Jan;43(1):218-25
[
8433562.001
]
[Cites]
Circulation. 1998 Sep 1;98(9):839-44
[
9738637.001
]
[Cites]
Pharmacol Res. 2002 Feb;45(2):147-54
[
11846628.001
]
[Cites]
Circulation. 1998 Mar 31;97(12):1129-35
[
9537338.001
]
[Cites]
J Am Soc Nephrol. 2003 Aug;14(8):2084-91
[
12874462.001
]
[Cites]
Am J Kidney Dis. 2003 Apr;41(4 Suppl 3):I-IV, S1-91
[
12671933.001
]
[Cites]
Free Radic Biol Med. 2002 Oct 15;33(8):1026-36
[
12374614.001
]
[Cites]
Am J Kidney Dis. 2002 Jun;39(6):1213-7
[
12046033.001
]
[Cites]
Kidney Int. 2002 Jan;61(1):297-304
[
11786112.001
]
[Cites]
Am J Kidney Dis. 2003 Mar;41(3):565-70
[
12612979.001
]
[Cites]
Kidney Int. 1997 Oct;52(4):1016-27
[
9328940.001
]
[Cites]
J Biol Chem. 1991 Jul 5;266(19):12216-22
[
1712015.001
]
[Cites]
Kidney Int. 2002 Nov;62(5):1524-38
[
12371953.001
]
[Cites]
N Engl J Med. 2004 Sep 23;351(13):1296-305
[
15385656.001
]
[Cites]
Nephrol Dial Transplant. 2002 Mar;17(3):347-8
[
11865072.001
]
[Cites]
Am J Kidney Dis. 1998 Jan;31(1):190-4
[
9428473.001
]
[Cites]
Circulation. 2001 Apr 17;103(15):1933-5
[
11306519.001
]
[Cites]
Circulation. 1999 Jul 20;100(3):230-5
[
10411845.001
]
[Cites]
J Am Soc Nephrol. 2003 Jun;14(6):1605-13
[
12761262.001
]
[Cites]
Clin Sci (Lond). 2003 Sep;105(3):251-66
[
12793855.001
]
[Cites]
N Engl J Med. 1995 Sep 7;333(10 ):621-7
[
7637722.001
]
[Cites]
Arterioscler Thromb Vasc Biol. 2001 Jul;21(7):1165-71
[
11451746.001
]
[Cites]
Atherosclerosis. 1999 Dec;147(2):253-61
[
10559511.001
]
[Cites]
Kidney Int. 2001 Jan;59(1):260-9
[
11135079.001
]
(PMID = 16157074.001).
[ISSN]
1522-6417
[Journal-full-title]
Current hypertension reports
[ISO-abbreviation]
Curr. Hypertens. Rep.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors
[Number-of-references]
50
61.
Harel Z, Perl J, Herzenberg AM, Bargman JM:
Inflammatory pseudotumor of the kidney allograft.
Am J Kidney Dis
; 2009 Sep;54(3):533-7
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[Title]
Inflammatory pseudotumor of the
kidney
allograft.
Inflammatory myofibroblastic
tumor
, or inflammatory pseudotumor, usually is a
benign
lesion composed of mixed inflammatory and fibroblastic elements.
It has rarely been reported in the posttransplantation setting and never in association with a
renal
allograft.
We report the first case of inflammatory myofibroblastic
tumor
infiltrating a
renal
allograft and highlight the role immunosuppression may have in the development of this lesion.
[MeSH-major]
Granuloma, Plasma Cell /
diagnosis
. Granuloma, Plasma Cell / pathology.
Kidney
Diseases /
diagnosis
.
Kidney
Diseases / pathology.
Kidney
Transplantation / adverse effects.
Kidney
Transplantation / pathology
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(PMID = 19376619.001).
[ISSN]
1523-6838
[Journal-full-title]
American journal of kidney diseases : the official journal of the National Kidney Foundation
[ISO-abbreviation]
Am. J. Kidney Dis.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
62.
Aregger F, Pilop C, Uehlinger DE, Brunisholz R, Carrel TP, Frey FJ, Frey BM:
Urinary proteomics before and after extracorporeal circulation in patients with and without acute kidney injury.
J Thorac Cardiovasc Surg
; 2010 Mar;139(3):692-700
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[Title]
Urinary proteomics before and after extracorporeal circulation in patients with and without acute
kidney
injury.
OBJECTIVE: Acute
kidney
injury is a well-known complication with high morbidity and mortality after cardiopulmonary bypass.
Cardiopulmonary bypass-associated acute
kidney
injury is still poorly understood.
Acute
kidney
injury was defined according to the RIFLE classification.
To identify differentially regulated proteins in acute
kidney
injury, we next compared the urinary proteome obtained on the first postoperative day between patients with and without acute
kidney
injury.
Acute
kidney
injury developed in 6 of 36 patients.
A modified urinary albumin was increased, and zinc-alpha-2-glycoprotein and a fragment of adrenomedullin-binding protein were decreased in patients with acute
kidney
injury.
Decreased excretion of zinc-alpha-2-glycoprotein in patients with acute
kidney
injury was confirmed by Western blot and enzyme-linked immunosorbent assay in an independent cohort of 22 patients with and 46 patients without acute
kidney
injury.
Zinc-alpha-2-glycoprotein is a potentially useful predictive marker for acute
kidney
injury after cardiopulmonary bypass surgery.
[MeSH-major]
Cardiopulmonary Bypass / adverse effects.
Kidney
Diseases / etiology.
Kidney
Diseases / urine. Proteomics
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.
NCI CPTC Antibody Characterization Program.
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.
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[Copyright]
Copyright 2010 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.
(PMID = 20176211.001).
[ISSN]
1097-685X
[Journal-full-title]
The Journal of thoracic and cardiovascular surgery
[ISO-abbreviation]
J. Thorac. Cardiovasc. Surg.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
63.
Bhosale P, Peungjesada S, Devine C, Balachandran A, Iyer R:
Role of magnetic resonance imaging as an adjunct to clinical staging in cervical carcinoma.
J Comput Assist Tomogr
; 2010 Nov-Dec;34(6):855-64
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Magnetic resonance imaging depicts the morphological details of the female pelvis and is useful for evaluating both
benign
and malignant cervical masses.
Clinical staging, as defined by FIGO (International Federation of Gynecologic Oncology), is based on the findings of physical examination, lesion biopsies, chest radiography, cystoscopy, and
renal
sonography and can be erroneous, depending on the stage of the disease, by 16% to 65%.
The prognosis of cervical cancer is determined not only by stage, but also by nodal status,
tumor
volume, and depth of invasion, none of which are included in the FIGO guidelines.
[MeSH-major]
Magnetic Resonance Imaging / methods. Uterine Cervical
Neoplasms
/ pathology
[MeSH-minor]
Contrast Media. Female. Humans. Lymphatic Metastasis / pathology.
Neoplasm
Staging. Sensitivity and Specificity
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.
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consumer health - MRI Scans
.
International Agency for Research on Cancer - Screening Group.
diagnostics - Histopathology and cytopathology of the uterine cervix - digital atlas
.
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(PMID = 21084900.001).
[ISSN]
1532-3145
[Journal-full-title]
Journal of computer assisted tomography
[ISO-abbreviation]
J Comput Assist Tomogr
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Contrast Media
64.
Can B, Kulaksiz Erkmen G, Dalmizrak O, Ogus IH, Ozer N:
Purification and characterisation of rat kidney glutathione reductase.
Protein J
; 2010 May;29(4):250-6
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[Title]
Purification and characterisation of rat
kidney
glutathione reductase.
Kidney
and liver tissues were considered as a rich source of GR.
In this study, rat
kidney
GR was purified and some of its properties were investigated.
NADH was used as a coenzyme by rat
kidney
GR but with a lower efficiency (32.7%) than NADPH.
An optimum pH of 6.5 and optimum temperature of 65 degrees C were found for rat
kidney
GR.
[MeSH-major]
Glutathione Reductase / chemistry. Glutathione Reductase / metabolism.
Kidney
/ enzymology
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[Cites]
Mol Cell Biochem. 2007 Mar;297(1-2):139-49
[
17075686.001
]
[Cites]
Anal Biochem. 1981 Sep 15;116(2):531-6
[
7316181.001
]
[Cites]
J Bacteriol. 1984 Apr;158(1):317-24
[
6425264.001
]
[Cites]
J Nutr. 2004 Mar;134(3):489-92
[
14988435.001
]
[Cites]
Nature. 1970 Aug 15;227(5259):680-5
[
5432063.001
]
[Cites]
Biochem J. 1987 Aug 1;245(3):875-80
[
3311037.001
]
[Cites]
Biochemistry. 1990 Jun 19;29(24):5790-6
[
2200516.001
]
[Cites]
Science. 1983 Apr 29;220(4596):472-7
[
6836290.001
]
[Cites]
J Biol Chem. 1986 Feb 5;261(4):1629-35
[
3003077.001
]
[Cites]
Eur J Biochem. 1996 Jan 15;235(1-2):345-50
[
8631352.001
]
[Cites]
Biochemistry. 1982 Dec 21;21(26):6628-33
[
7159551.001
]
[Cites]
J Exp Bot. 2002 May;53(372):1283-304
[
11997376.001
]
[Cites]
FEBS Lett. 1989 Jun 19;250(1):72-4
[
2737302.001
]
[Cites]
Blood. 1963 May;21:573-85
[
13967896.001
]
[Cites]
Protist. 2010 Jan;161(1):91-101
[
19664954.001
]
[Cites]
Eur J Biochem. 1979 Aug 1;98(2):487-99
[
39757.001
]
[Cites]
J Biol Chem. 1975 Jul 25;250(14):5475-80
[
237922.001
]
[Cites]
J Biol Chem. 1968 Feb 25;243(4):809-14
[
5638597.001
]
[Cites]
J Biol Chem. 1952 Jan;194(1):119-30
[
14927599.001
]
[Cites]
Protein Pept Lett. 2010 May;17(5):667-74
[
19702563.001
]
[Cites]
Methods Enzymol. 1985;113:484-90
[
3003504.001
]
[Cites]
EMBO Rep. 2006 Mar;7(3):271-5
[
16607396.001
]
[Cites]
Biochem J. 1987 Mar 1;242(2):511-5
[
3109393.001
]
[Cites]
Enzyme. 1991;45(3):121-4
[
1815946.001
]
[Cites]
Anal Biochem. 1976 May 7;72:248-54
[
942051.001
]
[Cites]
Pathol Biol (Paris). 1996 Jan;44(1):77-85
[
8734304.001
]
[Cites]
Brain Res. 1995 May 22;680(1-2):16-22
[
7663973.001
]
[Cites]
Protein Expr Purif. 1998 Jun;13(1):41-4
[
9631513.001
]
[Cites]
Biochem Med Metab Biol. 1991 Feb;45(1):65-73
[
2015111.001
]
[Cites]
Protein J. 2004 Jul;23(5):317-24
[
15328887.001
]
[Cites]
Plant Physiol. 1992 Sep;100(1):138-45
[
16652936.001
]
(PMID = 20490902.001).
[ISSN]
1875-8355
[Journal-full-title]
The protein journal
[ISO-abbreviation]
Protein J.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
[Chemical-registry-number]
53-59-8 / NADP; EC 1.8.1.7 / Glutathione Reductase; ULW86O013H / Glutathione Disulfide
65.
Leclerc E, Baudoin R, Corlu A, Griscom L, Luc Duval J, Legallais C:
Selective control of liver and kidney cells migration during organotypic cocultures inside fibronectin-coated rectangular silicone microchannels.
Biomaterials
; 2007 Apr;28(10):1820-9
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[Title]
Selective control of liver and
kidney
cells migration during organotypic cocultures inside fibronectin-coated rectangular silicone microchannels.
In this work, the behaviors of embryonic liver and
kidney
explants were studied inside rectangular polydimethylsiloxane (PDMS) microchannels.
In
kidney
monocultures, with and without fibronectin, we did not observe any migration inside the microchannels.
Contrary to liver cells,
kidney
cell migration was triggered when both fibronectin coating and coculture with liver or another
kidney
explant were used.
The migration was more largely observed in coculture with liver when compared to
kidney
-
kidney
cocultures.
In the case of liver-
kidney
coculture with fibronectin, the progression of the
kidney
cells inside the microchannels appears as a displacement of the entire
kidney
explant in the direction of the liver.
After contact, we observed a complete merging of both liver and
kidney
explants.
In contrast, for liver-
kidney
cocultures without fibronectin, only the liver moved toward
the kidney
.
[MeSH-major]
Fibronectins / pharmacology.
Kidney
/ cytology. Liver / cytology. Liver / growth & development. Liver, Artificial. Organ Culture Techniques / instrumentation. Tissue Engineering / instrumentation
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(PMID = 17178157.001).
[ISSN]
0142-9612
[Journal-full-title]
Biomaterials
[ISO-abbreviation]
Biomaterials
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Coated Materials, Biocompatible; 0 / Fibronectins; 0 / Silicones
66.
Santiago C, Lucha PA:
Atypical presentation of a retrorectal ancient schwannoma: a case report and review of the literature.
Mil Med
; 2008 Aug;173(8):814-6
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Retrorectal
tumors
are rare and frequently present either incidentally or with vague symptoms.
Schwannomas of the presacral region are one variant described as
benign
tumors of
neurogenic origin.
We present the case of a 37-year-old man presenting with symptoms of left
renal
colic, impotence, and left trochanteric pain.
The patient underwent an exploratory laparotomy with resection of the
tumor
, which subsequent analysis showed to be a schwannoma with ancient degenerative changes.
[MeSH-major]
Neurilemmoma /
diagnosis
. Rectal
Neoplasms
/
diagnosis
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.
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(PMID = 18751604.001).
[ISSN]
0026-4075
[Journal-full-title]
Military medicine
[ISO-abbreviation]
Mil Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
England
[Number-of-references]
15
67.
Anchi T, Tamura K, Inoue K, Ashida S, Yamasaki I, Takeuchi T, Shuin T:
[A case of carcinoid tumor arising from a horseshoe kidney].
Hinyokika Kiyo
; 2009 Jun;55(6):327-30
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[Title]
[A case of carcinoid
tumor
arising from a horseshoe
kidney
].
Carcinoid
tumor
of the
kidney
is an extremely rare
neoplasm
.
We report a case of primary carcinoid
tumor
arising from a horseshoe
kidney
in a 31-year-old man.
From the results of computed tomography, magnetic resonance imaging and angiography, we suspected
renal tumor
arising from a horseshoe
kidney
and performed left partial nephrectomy with isthmectomy.
Pathological findings of hematoxylin eosin staining revealed
tumor
cells proliferating in a cord-like and ribbon-like structure and the
tumor
cells stained strongly for chromogranin A, grimelius and neuron specific enolase.
According to these findings, we diagnosed carcinoid
tumor
arising from a horseshoe
kidney
.
[MeSH-major]
Carcinoid
Tumor
/ etiology.
Kidney
/ abnormalities.
Kidney Neoplasms
/ etiology
Genetic Alliance.
consumer health - Carcinoid Tumor
.
Genetic Alliance.
consumer health - Horseshoe kidney
.
MedlinePlus Health Information.
consumer health - Carcinoid Tumors
.
MedlinePlus Health Information.
consumer health - Kidney Cancer
.
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.
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(PMID = 19588864.001).
[ISSN]
0018-1994
[Journal-full-title]
Hinyokika kiyo. Acta urologica Japonica
[ISO-abbreviation]
Hinyokika Kiyo
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
68.
Astigueta JC, Abad MA, Pow-Sang MR, Morante C, Meza L, Destefano V, Dyer R:
Epithelioid angiomyolipoma: a rare variant of renal angiomyolipoma.
Arch Esp Urol
; 2009 Jul;62(6):493-7
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[Title]
Epithelioid angiomyolipoma: a rare variant of
renal
angiomyolipoma.
OBJECTIVE: We present a case of primary
renal
epithelioid angiomyolipoma, its association with tuberous sclerosis and review the literature.
CT scan of the abdomen showed the presence of a left
renal tumor
.
Pathologic study of the specimen showed primary
renal
epithelioid angiomyolipoma, corroborated by immunohistochemistry staining.
CONCLUSIONS:
Renal
angiomyolipoma is an uncommon
benign tumor
, representing a challenge for clinical and pathological
diagnosis
.
[MeSH-major]
Angiomyolipoma / pathology.
Kidney Neoplasms
/ pathology
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.
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NCI CPTAC Assay Portal
.
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(PMID = 19736381.001).
[ISSN]
1576-8260
[Journal-full-title]
Archivos españoles de urología
[ISO-abbreviation]
Arch. Esp. Urol.
[Language]
eng; spa
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Spain
[Number-of-references]
15
69.
Crane HM, Kestenbaum B, Harrington RD, Kitahata MM:
Amprenavir and didanosine are associated with declining kidney function among patients receiving tenofovir.
AIDS
; 2007 Jul 11;21(11):1431-9
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[Title]
Amprenavir and didanosine are associated with declining
kidney
function among patients receiving tenofovir.
OBJECTIVE: To examine the effect of antiretroviral agents and clinical factors on the development of tenofovir-associated
kidney
dysfunction.
Patients'
kidney
function prior to initiating and while receiving tenofovir was evaluated in relation to other antiretroviral medications and demographic and clinical characteristics.
Decline in
kidney
function was assessed by the glomerular filtration rate (GFR) as estimated by the Cockcroft-Gault (CG) equation, which incorporates weight.
Secondary analyses used the simplified Modification of Diet in
Renal
Disease (MDRD) equation.
RESULTS: Among the 445 patients initiating tenofovir, 51 (11%) developed a decline in
kidney
function.
In multivariate analysis, there was a significant association between decline in
kidney
function and concurrent use of amprenavir [odds ratio (OR) 3.6; P = 0.045] and didanosine (OR, 3.1; P = 0.006), age over 50 years (OR, 4.4; P = 0.03), and lower baseline weight (OR, 0.95/kg; P < 0.001).
Patients identified with
kidney
dysfunction by the MDRD equation did not fully overlap with those identified by the CG equation.
CONCLUSIONS: Didanosine and amprenavir use, increased age, and lower baseline weight were significantly associated with risk for
kidney
dysfunction among patients receiving tenofovir.
[MeSH-minor]
Adult. Age Factors. Analysis of Variance. Antiretroviral Therapy, Highly Active. Body Weight. Carbamates / adverse effects. Carbamates / therapeutic use. Creatinine / urine. Didanosine / adverse effects. Didanosine / therapeutic use. Drug Interactions. Female. Glomerular Filtration Rate / drug effects. Humans.
Kidney
/ drug effects.
Kidney
/ metabolism. Linear Models. Male. Middle Aged. Sulfonamides / adverse effects. Sulfonamides / therapeutic use. Tenofovir. Time Factors
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.
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author profiles
.
HIV InSite.
treatment guidelines - Renal Manifestations of HIV
.
Hazardous Substances Data Bank.
AMPRENAVIR
.
Hazardous Substances Data Bank.
DIDEOXYINOSINE
.
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[CommentIn]
AIDS. 2007 Nov 30;21(18):2566
[
18025906.001
]
(PMID = 17589189.001).
[ISSN]
0269-9370
[Journal-full-title]
AIDS (London, England)
[ISO-abbreviation]
AIDS
[Language]
eng
[Grant]
United States / NIAID NIH HHS / AI / AI-060464; United States / NIAID NIH HHS / AI / AI-27757
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Anti-HIV Agents; 0 / Carbamates; 0 / Organophosphonates; 0 / Sulfonamides; 5S0W860XNR / amprenavir; 99YXE507IL / Tenofovir; AYI8EX34EU / Creatinine; JAC85A2161 / Adenine; K3GDH6OH08 / Didanosine
70.
Montgomery RA, Zachary AA, Ratner LE, Segev DL, Hiller JM, Houp J, Cooper M, Kavoussi L, Jarrett T, Burdick J, Maley WR, Melancon JK, Kozlowski T, Simpkins CE, Phillips M, Desai A, Collins V, Reeb B, Kraus E, Rabb H, Leffell MS, Warren DS:
Clinical results from transplanting incompatible live kidney donor/recipient pairs using kidney paired donation.
JAMA
; 2005 Oct 5;294(13):1655-63
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[Title]
Clinical results from transplanting incompatible live
kidney
donor/recipient pairs using
kidney
paired donation.
CONTEXT: First proposed 2 decades ago, live
kidney
paired donation (KPD) was considered a promising new approach to addressing the shortage of organs for transplantation.
DESIGN, SETTING, AND PATIENTS: Prospective series of paired donations matched and transplanted from a pool of blood type or crossmatch incompatible donors and recipients with end-stage
renal
disease (6 conventional and 4 unconventional KPD transplants) at a US tertiary referral center (between June 2001 and November 2004) with expertise in performing transplants in patients with high immunologic risk.
INTERVENTION:
Kidney
paired donation and live donor
renal
transplantation.
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[CommentIn]
JAMA. 2005 Oct 5;294(13):1691-3
[
16204670.001
]
(PMID = 16204665.001).
[ISSN]
1538-3598
[Journal-full-title]
JAMA
[ISO-abbreviation]
JAMA
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
71.
Nakamura Y, Urashima M, Nishihara R, Matsuura A, Bekku K, Iguchi H, Uesugi T, Saegusa M, Aramaki K:
Inflammatory pseudotumor of the kidney with renal artery penetration.
Radiat Med
; 2007 Dec;25(10):541-7
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[Title]
Inflammatory pseudotumor of the
kidney
with
renal
artery penetration.
Inflammatory pseudotumor (IPT) is a quasineoplastic lesion that most commonly involves the lung and the orbit;
kidney
involvement is rare.
We report a case of inflammatory pseudotumor of the
kidney
.
Nonenhanced computed tomography (CT) demonstrated an ill-defined, isodensity mass measuring 3.5 cm in the lower portion of the left
kidney
.
Contrast-enhanced CT showed that branches of the
renal
artery without encasement penetrated the
tumor
; there was a little enhancement in the mass on the arterial phase and homogeneous enhancement on the venous phase.
Most IPTs of the
kidney
appear as an ill-defined, hypovascular, homogeneous
tumor
on CT images, with variable signal intensity on MRI T1WIs and low signal intensity on T2WIs.
Our case had the same imaging findings, with branches of the
renal
artery penetrating the
tumor
.
If the
renal tumor
has these radiological findings, the
tumor
may be IPT.
[MeSH-major]
Granuloma, Plasma Cell / pathology.
Kidney
Diseases / pathology.
Renal
Artery / pathology
[MeSH-minor]
Diagnosis
, Differential. Humans. Magnetic Resonance Imaging. Male. Middle Aged.
Neoplasm
Invasiveness. Tomography, X-Ray Computed
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[Cites]
Arch Esp Urol. 2002 Jan-Feb;55(1):85-7
[
11957761.001
]
[Cites]
Acta Cytol. 2000 May-Jun;44(3):478-80
[
10834015.001
]
[Cites]
Int J Urol. 2004 May;11(5):337-9
[
15147553.001
]
[Cites]
Actas Urol Esp. 2003 Oct;27(9):739-41
[
14626687.001
]
[Cites]
Int Urol Nephrol. 2004;36(2):141-3
[
15368680.001
]
[Cites]
Prog Urol. 2003 Feb;13(1):135-9
[
12703371.001
]
[Cites]
Arch Esp Urol. 2003 May;56(4):428-30
[
12830617.001
]
[Cites]
Am J Nephrol. 2000 May-Jun;20(3):217-21
[
10878405.001
]
[Cites]
AJR Am J Roentgenol. 1996 May;166(5):1151-5
[
8615260.001
]
[Cites]
Am J Surg Pathol. 2003 May;27(5):658-66
[
12717250.001
]
[Cites]
Int J Urol. 1999 Feb;6(2):107-10
[
10226817.001
]
[Cites]
Am J Kidney Dis. 1998 Jun;31(6):E5
[
10074585.001
]
[Cites]
J Urol. 1972 Jun;107(6):938-9
[
5033977.001
]
[Cites]
J Thorac Surg. 1954 Jul;28(1):55-63
[
13175281.001
]
[Cites]
Hinyokika Kiyo. 2004 Sep;50(9):629-31
[
15518129.001
]
[Cites]
Hinyokika Kiyo. 2006 Jan;52(1):31-3
[
16479987.001
]
[Cites]
South Med J. 1998 Nov;91(11):1050-3
[
9824189.001
]
[Cites]
Br J Urol. 1990 May;65(5):548-9
[
2354326.001
]
[Cites]
Verh Dtsch Ges Pathol. 1998;82:75-82
[
10095420.001
]
[Cites]
AJR Am J Roentgenol. 1976 Jun;126(6):1197-1202
[
179381.001
]
[Cites]
Bone Marrow Transplant. 2004 Nov;34(9):831-2
[
15322569.001
]
[Cites]
Radiographics. 2003 May-Jun;23(3):719-29
[
12740472.001
]
[Cites]
Rev Med Interne. 2000 Oct;21(10):889-92
[
11075397.001
]
[Cites]
Ann Urol (Paris). 2001 Jan;35(1):30-3
[
11233317.001
]
[Cites]
Radiology. 2005 Aug;236(2):441-50
[
16040900.001
]
[Cites]
J Urol. 1982 Jun;127(6):1177-8
[
7087029.001
]
[Cites]
Hinyokika Kiyo. 2000 Jan;46(1):23-6
[
10723660.001
]
[Cites]
AJR Am J Roentgenol. 1990 Oct;155(4):713-22
[
2119098.001
]
[Cites]
Nihon Hinyokika Gakkai Zasshi. 2001 Jul;92(5):589-92
[
11517572.001
]
[Cites]
Actas Urol Esp. 2005 Sep;29(8):794-6
[
16304914.001
]
[Cites]
Urology. 1976 Jul;8(1):89-91
[
941370.001
]
[Cites]
Surg Today. 2006;36(8):710-3
[
16865515.001
]
[Cites]
Int Urol Nephrol. 2004;36(2):137-40
[
15368679.001
]
[Cites]
Korean J Radiol. 2000 Oct-Dec;1(4):219-22
[
11752959.001
]
[Cites]
Ann Urol (Paris). 2003 Aug;37(4):147-9
[
12951701.001
]
[Cites]
Arch Pathol Lab Med. 2000 Aug;124(8):1209-12
[
10923085.001
]
[Cites]
Pediatr Pathol. 1992 Jul-Aug;12 (4):557-61
[
1409154.001
]
(PMID = 18085406.001).
[ISSN]
0288-2043
[Journal-full-title]
Radiation medicine
[ISO-abbreviation]
Radiat Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
72.
Arija I, Centeno C, Viveros A, Brenes A, Marzo F, Illera JC, Silvan G:
Nutritional evaluation of raw and extruded kidney bean (Phaseolus vulgaris L. var. pinto) in chicken diets.
Poult Sci
; 2006 Apr;85(4):635-44
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[Title]
Nutritional evaluation of raw and extruded
kidney
bean (Phaseolus vulgaris L. var. pinto) in chicken diets.
An experiment was conducted to study the effect of inclusion of different concentrations (0, 100, 200, and 300 g/kg) of raw
kidney
bean and extruded
kidney
bean in broiler chick (0 to 21 d of age) diets on performance, digestive organ sizes, protein and amino acid digestibilities, intestinal viscosity, cecal pH, and blood parameters.
Data were analyzed as a 3 x 2 factorial arrangement with 3 levels
of kidney
bean with and without extrusion.
Positive control without
kidney
bean was used.
Increasing
the kidney
bean content in the diet reduced weight gain and consumption, and increased the feed-to-gain ratio.
Relative pancreas, liver, and jejunum weights, and intestinal viscosity were increased in response to increasing
kidney
bean concentration in the diet.
The inclusion of different concentrations
of kidney
bean did not affect the apparent ileal digestibility of essential and nonessential amino acids, except for Met, Phe, and Cys, which were increased.
Increasing
kidney
bean in the diet did not affect blood parameters, except for total protein, which was increased, and for androstenedione and testosterone, which were reduced.
We concluded that the inclusion
of kidney
bean in chicken diets cause a negative effect on performance and CP and amino acid digestibilities, and modified digestive organ sizes, intestinal viscosity, cecal pH, and some blood parameters.
These effects were counteracted by the extrusion
of kidney
bean.
However, the inclusion of extruded
kidney
bean in a chick diet resulted in poorer performance compared with that obtained with a corn-soybean diet.
NCI CPTAC Assay Portal.
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NCI CPTC Antibody Characterization Program.
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(PMID = 16615347.001).
[ISSN]
0032-5791
[Journal-full-title]
Poultry science
[ISO-abbreviation]
Poult. Sci.
[Language]
eng
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Plant Preparations
73.
Al-Bazzaz PH:
Kidney transplantation in Erbil, Iraq: a single-center experience.
Saudi J Kidney Dis Transpl
; 2010 Mar;21(2):359-62
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[Title]
Kidney
transplantation in Erbil, Iraq: a single-center experience.
Kidney
transplantation is associated with improved quality of life and better survival among patients with end-stage
renal
disease.
The aim of this study is to assess the experience
of kidney
transplant program in a single center in Erbil, Iraq.
The records of 83 pairs, donors and recipients, treated with
kidney
transplantation at the Zheen Hospital in Erbil, over a two-year period were collected and analyzed.
In conclusion, even though experience related to
kidney
transplantation in Erbil is limited, the reported results are encouraging for a promising future.
[MeSH-major]
Kidney
Failure, Chronic / surgery.
Kidney
Transplantation. Tissue Donors / supply & distribution
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Kidney Failure
.
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.
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(PMID = 20228533.001).
[ISSN]
1319-2442
[Journal-full-title]
Saudi journal of kidney diseases and transplantation : an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia
[ISO-abbreviation]
Saudi J Kidney Dis Transpl
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Saudi Arabia
74.
Musquera Felip M, Peri Cusí L, Alcaraz Asensio A:
[Surgical aspects of living-donor kidney transplantation].
Nefrologia
; 2010;30 Suppl 2:71-9
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[Title]
[Surgical aspects of living-donor
kidney
transplantation].
For these reasons, we can accept laparoscopic
kidney
living donor nephrectomy as the gold standard surgical technique in these patients.
In order to decide which
kidney
is better to extract, it is mandatory to maintain the best
kidney
in the donor.
[MeSH-major]
Kidney
Transplantation. Living Donors. Nephrectomy / methods
Genetic Alliance.
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.
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consumer health - Kidney Transplantation
.
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.
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(PMID = 21183965.001).
[ISSN]
0211-6995
[Journal-full-title]
Nefrología : publicación oficial de la Sociedad Española Nefrologia
[ISO-abbreviation]
Nefrologia
[Language]
spa
[Publication-type]
English Abstract; Journal Article; Randomized Controlled Trial
[Publication-country]
Spain
75.
Petrovic V, Jovanovic I, Pesic I, Stefanovic V:
Role of stem cells in kidney repair.
Ren Fail
; 2010;32(10):1237-44
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[Title]
Role of stem cells in
kidney
repair.
End-stage
renal
disease and acute
renal
failure are the most important issues of practical and clinical nephrology, bearing in mind their high mortality rate, solely symptomatic treatment, and overall economic impact on society.
The advances in stem cell biology opened the door for the new era in treatment of many disorders, including
renal
, offering new therapeutical solutions.
Findings suggesting that the adult
kidney
contains stem cells and that stem cells from bone marrow have potential to differentiate into
renal
cells focused research on the possible application of these cells in therapy
of kidney
disorders.
The other promising candidates for stem cell therapy for
the kidney
are embryonic stem cells and amniotic fluid-derived stem cells.
[MeSH-major]
Kidney
Failure, Chronic / surgery
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(PMID = 20954989.001).
[ISSN]
1525-6049
[Journal-full-title]
Renal failure
[ISO-abbreviation]
Ren Fail
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
76.
Qiao H, Bai J, Chen Y, Tian J:
Kidney modelling for FDG excretion with PET.
Int J Biomed Imaging
; 2007;2007:63234
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[Title]
Kidney
modelling for FDG excretion with PET.
The filtration process in
kidney
can be seen in the sequential images of each study.
Variational distribution of FDG in
kidney
can be detected in dynamic data.
According to the structure and function,
kidney
is divided into parenchyma and pelvis.
A unidirectional three-compartment model is proposed to describe the
renal
function in FDG excretion.
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[Cites]
J Nucl Med. 1999 Aug;40(8):1352-7
[
10450688.001
]
[Cites]
J Nucl Med. 1999 Aug;40(8):1358-66
[
10450689.001
]
[Cites]
J Nucl Med. 2002 Oct;43(10):1331-8
[
12368371.001
]
[Cites]
J Nucl Med. 2003 Jul;44(7):1113-47
[
12843230.001
]
[Cites]
Am J Physiol. 1980 Jan;238(1):E69-82
[
6965568.001
]
(PMID = 17728841.001).
[ISSN]
1687-4188
[Journal-full-title]
International journal of biomedical imaging
[ISO-abbreviation]
Int J Biomed Imaging
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC1950229
77.
Nemati E, Pourfarziani V, Jafari AM, Assari S, Moghani-Lankarani M, Khedmat H, Bagheri N, Saadat SH:
Prediction of inpatient survival and graft loss in rehospitalized kidney recipients.
Transplant Proc
; 2007 May;39(4):974-7
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[Title]
Prediction of inpatient survival and graft loss in rehospitalized
kidney
recipients.
INTRODUCTION: Despite a sizeable amount of research conducted hitherto into predictors of
renal
transplantation outcomes, there are scarce, data on predictors of in-hospital outcomes of post-
kidney
transplant rehospitalization.
This study sought to provide a user-friendly prediction model for inpatient mortality and graft loss among rehospitalized
kidney
recipients.
METHOD: This retrospective review of 424 consecutive
kidney
recipients rehospitalized after
kidney
transplantation between the years 2000 and 2005 used multiple logistic regression analysis to evaluate predictors of hospitalization outcomes.
RESULTS: Multivariate analysis showed that age at admission, diabetes mellitus as the cause of end-stage
renal
disease (ESRD), admission due to cerebrovascular accident (CVA), surgical complications were predictors of in-hospital death; age at transplantation, surgical complications, and rejection were predictors of graft loss.
CONCLUSIONS: Our prediction equations, using simple demographic and clinical variables, estimated the probability of inpatient mortality and graft loss among re-hospitalized
kidney
recipients.
[MeSH-major]
Graft Survival / physiology. Hospital Mortality. Inpatients / statistics & numerical data.
Kidney
Transplantation / physiology. Patient Readmission / statistics & numerical data
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(PMID = 17524866.001).
[ISSN]
0041-1345
[Journal-full-title]
Transplantation proceedings
[ISO-abbreviation]
Transplant. Proc.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
78.
Jeon HG, Lee SR, Kim KH, Oh YT, Cho NH, Rha KH, Yang SC, Han WK:
Benign lesions after partial nephrectomy for presumed renal cell carcinoma in masses 4 cm or less: prevalence and predictors in Korean patients.
Urology
; 2010 Sep;76(3):574-9
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[Title]
Benign
lesions after partial nephrectomy for presumed
renal
cell carcinoma in masses 4 cm or less: prevalence and predictors in Korean patients.
OBJECTIVES: To investigate the prevalence and predictors associated with
benign
lesions in Korean patients after partial nephrectomy for presumed
renal
cell carcinoma (RCC) for lesions measuring ≤ 4 cm.
METHODS: We retrospectively investigated the medical records of 376 patients who underwent partial nephrectomy for presumed RCC with
renal
masses of size ≤ 4 cm between June 1997 and December 2008.
Demographic and clinicopathologic parameters were compared between
benign
lesions and RCC.
Logistic regression was done to identify parameters associated with
benign
lesions.
RESULTS: In the 376 patients, 81
tumors
(21.5%) were
benign
, including 35 angiomyolipomas (9.3%), 26 complicated cysts (6.9%), 11 oncocytomas (2.9%), and 9 others (2.4%).
Univariate analysis showed that time of surgery, female sex, younger age, and normal body mass index (body mass index (BMI) < 23 kg/m(2)) were associated with
benign
pathologic findings.
On multiple logistic regression analysis, female sex (OR, 4.91; 95% CI, 2.76-08.75; P < .001), age (OR, 0.97; 95% CI, 0.95-0.99; P = .009), and time of surgery (OR, 0.33; 95% CI, 0.11-0.95; P = .040) were independent predictors of
benign
histologic features.
Tumor
size, incidental
diagnosis
, and BMI were not significant predictors (P > .05).
CONCLUSIONS: Our study with a large cohort of Asian patients showed that the prevalence of
benign
lesions was similar to previously reported Western studies.
However, the most common
benign
lesion was angiomyolipoma, compared with oncocytoma in Western countries.
The results of this study may help clinicians counsel female and younger patients recently diagnosed with small
renal
masses and decide the most appropriate treatment, including
renal
biopsies and close observation.
[MeSH-major]
Carcinoma,
Renal
Cell / epidemiology. Carcinoma,
Renal
Cell / pathology.
Kidney Neoplasms
/ epidemiology.
Kidney Neoplasms
/ pathology. Nephrectomy
Genetic Alliance.
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.
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.
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[Copyright]
Copyright © 2010 Elsevier Inc. All rights reserved.
[CommentIn]
Urology. 2010 Sep;76(3):579
[
20832606.001
]
(PMID = 20303148.001).
[ISSN]
1527-9995
[Journal-full-title]
Urology
[ISO-abbreviation]
Urology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
79.
Zhang X, Li HZ, Ma X, Zheng T, Li LC, Ye ZQ:
Retroperitoneal laparoscopic nephron-sparing surgery for renal tumors: report of 32 cases.
Urology
; 2005 Jun;65(6):1080-4; discussion 1084-5
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[Title]
Retroperitoneal laparoscopic nephron-sparing surgery for
renal
tumors
: report of 32 cases.
OBJECTIVES: To evaluate the feasibility and clinical efficacy of retroperitoneal laparoscopic nephron-sparing surgery for
renal
tumors
.
METHODS: Between June 2002 and February 2004, 11 cases of
renal benign tumor
and 21 cases of
renal
malignant
tumor
underwent enucleation of the
tumor
and wedge resection of the
tumor
through retroperitoneal laparoscopy, respectively.
Tumor
resection and hemostasis were mainly achieved by harmonic scalpel.
Follow-up studies were performed with an evaluation using
renal
spiral computed tomography.
The pathologic examination confirmed
renal
cell carcinoma in 21 patients and angiomyolipoma in 11.
The pathologic stage was pT1a in the 21 patients with
renal
cell carcinoma.
All resected
tumor
specimens had negative surgical margins for cancer.
CONCLUSIONS: Our results indicate that retroperitoneal laparoscopic nephron-sparing surgery represents a feasible option for patients with localized
renal
tumors
.
This procedure could offer precise and complete
tumor
excision while minimizing morbidity, improving cosmesis, and shortening convalescence.
[MeSH-major]
Kidney Neoplasms
/ surgery. Laparoscopy. Nephrectomy / methods
[MeSH-minor]
Adult. Angiomyolipoma / surgery. Carcinoma,
Renal
Cell / surgery. Female. Humans. Male. Middle Aged
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(PMID = 15913730.001).
[ISSN]
1527-9995
[Journal-full-title]
Urology
[ISO-abbreviation]
Urology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
80.
Hilhorst MT, Kranenburg LW, Busschbach JJ:
Should health care professionals encourage living kidney donation?
Med Health Care Philos
; 2007 Mar;10(1):81-90
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[Title]
Should health care professionals encourage living
kidney
donation?
Living
kidney
donation provides a promising opportunity in situations where the scarcity of cadaveric
kidneys
is widely acknowledged.
While many patients and their relatives are willing to accept its benefits, others are concerned about living
kidney
programs; they appear to feel pressured into accepting living
kidney
transplantations as the only proper option for them.
Evidence suggests that both patients and their relatives have attitudes towards living
kidney
donation that are often open to change and, accordingly, can be influenced.
[MeSH-major]
Counseling / ethics.
Kidney
Transplantation / psychology. Living Donors / psychology. Physician-Patient Relations / ethics. Professional-Family Relations / ethics
MedlinePlus Health Information.
consumer health - Choosing a Doctor or Health Care Service
.
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.
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.
MedlinePlus Health Information.
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.
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[Cites]
Health Policy. 1998 Jun;44(3):215-32
[
10182294.001
]
[Cites]
Transpl Int. 2005 May;18(5):519-23
[
15819799.001
]
[Cites]
JAMA. 2005 Apr 20;293(15):1883-90
[
15840863.001
]
[Cites]
J Med Ethics. 2005 Jun;31(6):362-5
[
15923488.001
]
[Cites]
Transplantation. 2005 Jun 15;79(11):1470-4
[
15940033.001
]
[Cites]
Ethical Theory Moral Pract. 2005 Apr;8(1-2):197-215
[
16459404.001
]
[Cites]
Transplantation. 2004 Jul 27;78(2):194-7
[
15280677.001
]
[Cites]
Med Health Care Philos. 2002;5(1):53-63
[
11954994.001
]
[Cites]
Med Health Care Philos. 2002;5(2):199-204
[
12168995.001
]
[Cites]
JAMA. 2002 Oct 2;288(13):1589-93
[
12350189.001
]
[Cites]
J Med Ethics. 2003 Jun;29(3):142-6
[
12796432.001
]
[Cites]
Transplantation. 2003 Nov 27;76(10):1437-44
[
14657682.001
]
[Cites]
Nephrol Dial Transplant. 2004 Jun;19(6):1600-5
[
15004261.001
]
[Cites]
Kennedy Inst Ethics J. 2001 Sep;11(3):285-303
[
11700684.001
]
(PMID = 16847727.001).
[ISSN]
1386-7423
[Journal-full-title]
Medicine, health care, and philosophy
[ISO-abbreviation]
Med Health Care Philos
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Other-IDs]
NLM/ PMC2778634
81.
Lin SY, Liu WY, Chen WC, Chen RH:
Secondary hypertension due to a renin-secreting juxtaglomerular cell tumor.
J Formos Med Assoc
; 2010 Mar;109(3):237-40
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[Title]
Secondary hypertension due to a renin-secreting juxtaglomerular cell
tumor
.
A juxtaglomerular cell
tumor
(JCT) is a rare, renin-secreting
tumor
of the
kidney
and can cause hypertension.
JCT is pathologically
benign
, and resection of the
tumor
is curative for hypertension.
Abdominal computed tomography disclosed a 2 cm solid mass in the left
kidney
.
However,
renal
vein sampling and captopril test results were equivocal.
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.
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[Copyright]
2010 Formosan Medical Association & Elsevier. Published by Elsevier B.V. All rights reserved.
(PMID = 20434032.001).
[ISSN]
0929-6646
[Journal-full-title]
Journal of the Formosan Medical Association = Taiwan yi zhi
[ISO-abbreviation]
J. Formos. Med. Assoc.
[Language]
ENG
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Singapore
[Chemical-registry-number]
EC 3.4.23.15 / Renin
82.
Kageyama S, Tsuru T, Okamoto K, Narita M, Okada Y:
Primary synovial sarcoma arising from a crossed ectopic kidney with fusion.
Int J Urol
; 2010 Jan;17(1):96-8
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[Title]
Primary synovial sarcoma arising from a crossed ectopic
kidney
with fusion.
Crossed
renal
ectopia with fusion is a rare anomaly of the
kidney
.
The present case report describes a 67-year-old man with
renal tumor
who had been diagnosed as having a crossed ectopic
kidney
with fusion for 25 years.
The pathological
diagnosis of
the primary
tumor
specimen was Wilms'
tumor
with favorable histology.
Upon
tumor
recurrence, molecular detection of SYT-SSX2 fusion transcripts lead to
the diagnosis
of synovial sarcoma of the
kidney
.
To our knowledge, this is the first case of primary synovial sarcoma arising from a crossed ectopic
kidney
with fusion.
[MeSH-major]
Kidney
/ abnormalities.
Kidney Neoplasms
/ complications. Sarcoma, Synovial / complications
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(PMID = 20377831.001).
[ISSN]
1442-2042
[Journal-full-title]
International journal of urology : official journal of the Japanese Urological Association
[ISO-abbreviation]
Int. J. Urol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Australia
83.
Misra S, Gordon JD, Fu AA, Glockner JF, Chade AR, Mandrekar J, Lerman L, Mukhopadhyay D:
The porcine remnant kidney model of chronic renal insufficiency.
J Surg Res
; 2006 Oct;135(2):370-9
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[Title]
The porcine remnant
kidney
model of chronic
renal
insufficiency.
BACKGROUND: The purpose of the present study was to develop and characterize a porcine model of chronic
renal
insufficiency created by
renal
artery embolization.
In the pilot group, the embolization procedure was optimized with respect to the size of polyvinyl acrylide (PVA) particles, coils, and amount
of kidney
embolized.
The animals were followed serially for 4 weeks after the embolization procedure to determine the
renal
function and hypertensive response.
RESULTS:
The kidney
function after the embolization was characterized by acute deterioration in
renal
function, followed by improvement, and "stable" chronic
renal
insufficiency with statistically significant elevation in creatinine and BUN being observed until day 42.
The remnant
kidney
developed fibrosis in the tublointerstitial compartment as it hypertrophied and increased its weight which remained significantly elevated after embolization.
CONCLUSIONS: A reproducible remnant
kidney
model of chronic
renal
insufficiency in pigs was developed.
In this model, stable
renal
insufficiency develops by 4 weeks that lasts until 12 weeks.
[MeSH-major]
Disease Models, Animal.
Kidney
/ pathology.
Renal
Insufficiency, Chronic / pathology
[MeSH-minor]
Angiography. Animals. Blood Pressure. Blood Urea Nitrogen. Creatinine / metabolism. Male. Organ Size.
Renal
Artery Obstruction / surgery. Sus scrofa. Time Factors
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(PMID = 16815448.001).
[ISSN]
0022-4804
[Journal-full-title]
The Journal of surgical research
[ISO-abbreviation]
J. Surg. Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
AYI8EX34EU / Creatinine
84.
Yang B, Sonawane ND, Zhao D, Somlo S, Verkman AS:
Small-molecule CFTR inhibitors slow cyst growth in polycystic kidney disease.
J Am Soc Nephrol
; 2008 Jul;19(7):1300-10
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[Title]
Small-molecule CFTR inhibitors slow cyst growth in polycystic
kidney
disease.
Cyst expansion in polycystic
kidney
disease (PKD) involves progressive fluid accumulation, which is believed to require chloride transport by the cystic fibrosis transmembrane conductance regulator (CFTR) protein.
These compounds also inhibited cyst number and growth by >80% in an embryonic
kidney
cyst model involving 4-d organ culture of embryonic day 13.5 mouse
kidneys
in 8-Br-cAMP-containing medium.
Subcutaneous delivery of tetrazolo-CFTR(inh)-172 and Ph-GlyH-101 to neonatal,
kidney
-specific PKD1 knockout mice produced stable, therapeutic inhibitor concentrations of >3 microM in urine and
kidney
tissue.
Treatment of mice for up to 7 d remarkably slowed
kidney
enlargement and cyst expansion and preserved
renal
function.
These results implicate CFTR in
renal
cyst growth and suggest that CFTR inhibitors may hold therapeutic potential to reduce cyst growth in PKD.
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[Cites]
Kidney Int. 1999 Apr;55(4):1187-97
[
10200981.001
]
[Cites]
Am J Kidney Dis. 1998 Dec;32(6):976-83
[
9856513.001
]
[Cites]
Clin Cancer Res. 2005 Oct 1;11(19 Pt 1):6924-32
[
16203784.001
]
[Cites]
FASEB J. 2006 Jan;20(1):130-2
[
16317066.001
]
[Cites]
J Nephrol. 2006 Jul-Aug;19(4):529-34
[
17048214.001
]
[Cites]
Cell Tissue Res. 2006 Dec;326(3):671-85
[
16767405.001
]
[Cites]
J Am Soc Nephrol. 2006 Dec;17(12):3424-37
[
17108316.001
]
[Cites]
J Am Soc Nephrol. 2007 May;18(5):1399-407
[
17429048.001
]
[Cites]
Gastroenterology. 2007 Apr;132(4):1234-44
[
17408659.001
]
[Cites]
Nat Genet. 2000 Jun;25(2):143-4
[
10835625.001
]
[Cites]
Annu Rev Med. 2001;52:93-123
[
11160770.001
]
[Cites]
J Am Soc Nephrol. 2002 Jul;13(7):1837-46
[
12089379.001
]
[Cites]
J Am Soc Nephrol. 2002 Sep;13(9):2384-98
[
12191984.001
]
[Cites]
J Clin Invest. 2002 Dec;110(11):1651-8
[
12464670.001
]
[Cites]
Kidney Int. 2003 Jan;63(1):365-76
[
12472805.001
]
[Cites]
N Engl J Med. 2004 Jan 8;350(2):151-64
[
14711914.001
]
[Cites]
Mol Genet Metab. 2004 Feb;81(2):75-85
[
14741187.001
]
[Cites]
FEBS Lett. 2004 Jan 30;558(1-3):52-6
[
14759515.001
]
[Cites]
Nat Med. 2004 Apr;10(4):363-4
[
14991049.001
]
[Cites]
J Gen Physiol. 2004 Aug;124(2):125-37
[
15277574.001
]
[Cites]
Kidney Int. 2004 Nov;66(5):1926-38
[
15496164.001
]
[Cites]
Scan Electron Microsc. 1986;(Pt 3):1135-50
[
3798016.001
]
[Cites]
Scanning Microsc. 1988 Sep;2(3):1739-63
[
3059485.001
]
[Cites]
Proc Natl Acad Sci U S A. 1989 Aug;86(15):6007-11
[
2474825.001
]
[Cites]
Trans Assoc Am Physicians. 1989;102:158-62
[
2561639.001
]
[Cites]
N Engl J Med. 1993 Jul 29;329(5):310-3
[
8321258.001
]
[Cites]
N Engl J Med. 1993 Jul 29;329(5):332-42
[
8321262.001
]
[Cites]
J Am Soc Nephrol. 1995 Oct;6(4):1230-41
[
8589291.001
]
[Cites]
Hum Mol Genet. 2008 Jun 1;17(11):1505-16
[
18263604.001
]
[Cites]
FASEB J. 1989 Dec;3(14):2629-32
[
2480260.001
]
[Cites]
Kidney Int. 1996 Jul;50(1):208-18
[
8807590.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10206-11
[
8816777.001
]
[Cites]
Eur J Clin Invest. 1996 Jun;26(6):506-13
[
8817166.001
]
[Cites]
Cell. 1996 Dec 13;87(6):979-87
[
8978603.001
]
[Cites]
Biochem J. 1997 Feb 15;322 ( Pt 1):259-65
[
9078271.001
]
[Cites]
Cell. 1998 Apr 17;93(2):177-88
[
9568711.001
]
[Cites]
Physiol Rev. 1998 Oct;78(4):1165-91
[
9790573.001
]
[Cites]
J Pharm Sci. 2005 Jan;94(1):134-43
[
15761937.001
]
(PMID = 18385427.001).
[ISSN]
1533-3450
[Journal-full-title]
Journal of the American Society of Nephrology : JASN
[ISO-abbreviation]
J. Am. Soc. Nephrol.
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / HL73856; United States / NIDDK NIH HHS / DK / P50 DK057328; United States / NEI NIH HHS / EY / R01 EY013574; United States / NIBIB NIH HHS / EB / R01 EB000415; United States / NIDDK NIH HHS / DK / R01 DK054053; United States / NIDDK NIH HHS / DK / DK57328; United States / NIDDK NIH HHS / DK / R01 DK035124; United States / NHLBI NIH HHS / HL / R01 HL073856; United States / NIDDK NIH HHS / DK / P30 DK072517; United States / NIDDK NIH HHS / DK / DK54053; United States / NIDDK NIH HHS / DK / DK72517; United States / NHLBI NIH HHS / HL / R01 HL059198; United States / NEI NIH HHS / EY / EY13574; United States / NIDDK NIH HHS / DK / DK35124; United States / NIBIB NIH HHS / EB / EB00415; United States / NHLBI NIH HHS / HL / HL59198; United States / NIDDK NIH HHS / DK / R37 DK035124; United States / NIBIB NIH HHS / EB / R37 EB000415
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cadherins; 0 / Cdh16 protein, mouse; 0 / TRPP Cation Channels; 0 / Thiazolidines; 0 / polycystic kidney disease 1 protein; 126880-72-6 / Cystic Fibrosis Transmembrane Conductance Regulator; 14379-80-7 / glycine hydrazide; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases; TE7660XO1C / Glycine
[Other-IDs]
NLM/ PMC2440296
85.
Wang Y, Wang Z, Wang W, Ren H, Zhang W, Chen N:
Analysis of factors associated with renal function in Chinese adults with congenital solitary kidney.
Intern Med
; 2010;49(20):2203-9
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[Title]
Analysis of factors associated with
renal
function in Chinese adults with congenital solitary
kidney
.
BACKGROUND: Patients with congenital solitary
kidney
have an increased risk of developing hypertension, proteinuria and
renal
insufficiency.
However, the specific factors associated with the progression of
renal
function in adults with congenital solitary
kidney
remain still unclear.
The purpose of this study was to identify factors that are independently associated with
renal
function progression in patients with congenital solitary
kidney
.
METHODS: Sixty-five Chinese adults with congenital solitary
kidney
(48 patients with unilateral
renal
agenesis and 17 with severe unilateral
renal
dysplasia) were recruited into our study retrospectively.
RESULTS: Of sixty-five patients with congenital solitary
kidney
, the prevalence of hypertension, proteinuria and
renal
insufficiency was 36.9%, 35.4% and 38.5%, respectively.
While there was no statistically significant difference in prevalence of hypertension between patients with and without
renal
insufficiency, the prevalence of proteinuria in patients with
renal
insufficiency was significantly higher than in those without
renal
insufficiency (p<0.05).
Logistic regression analysis revealed that
kidney
length and proteinuria were independently associated with the progression of
renal
function (OR=0.20, 95%CI 0.05-0.79, and OR=8.30, 95%CI 2.30-29.96, respectively).
CONCLUSION: Hypertension, proteinuria or
renal
insufficiency was present in approximately one-third of adults with congenital solitary
kidney
.
Those with a
kidney
length of less than 120 mm or proteinuria had a much higher risk of
renal
insufficiency.
[MeSH-major]
Hypertension,
Renal
/ etiology.
Kidney
/ abnormalities.
Kidney
Failure, Chronic / etiology. Proteinuria / etiology
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(PMID = 20962438.001).
[ISSN]
1349-7235
[Journal-full-title]
Internal medicine (Tokyo, Japan)
[ISO-abbreviation]
Intern. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers; 268B43MJ25 / Uric Acid; AYI8EX34EU / Creatinine
86.
Newsome BB, Warnock DG, Kiefe CI, Weissman NW, Houston TK, Centor RM, Person SD, McClellan WM, Allison JJ:
Delay in time to receipt of thrombolytic medication among Medicare patients with kidney disease.
Am J Kidney Dis
; 2005 Oct;46(4):595-602
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[Title]
Delay in time to receipt of thrombolytic medication among Medicare patients with
kidney
disease.
BACKGROUND: Patients with
kidney
disease and acute myocardial infarction (AMI) receive standard therapy, including thrombolytic medication, less frequently than patients with normal
kidney
function.
Our goal is to identify potential differences in thrombolytic medication delays and thrombolytic-associated bleeding events by severity
of kidney
disease.
Average time to thrombolytic therapy was longer in patients with worse
kidney
function.
Adjusted hazard ratios for minutes to thrombolytic therapy were 0.83 (95% confidence interval [CI], 0.79 to 0.87) for patients with a serum creatinine level of 1.6 to 2.0 mg/dL (141 to 177 micromol/L) and 0.58 (95% CI, 0.53 to 0.63) for patients with a creatinine level greater than 2.0 mg/dL (>177 micromol/L) or on dialysis therapy compared with those with normal
kidney
function.
Odds ratios for bleeding events in patients administered thrombolytics versus those who were not decreased with worse
kidney
function: adjusted odds ratios, 2.28 (95% CI, 2.16 to 2.42) in patients with normal
kidney
function and 1.84 (95% CI, 1.09 to 3.10) in dialysis patients.
CONCLUSION: Patients with worse
kidney
function experienced treatment delays, but were not at greater risk for thrombolysis-associated excess bleeding events.
[MeSH-major]
Fibrinolytic Agents / administration & dosage.
Kidney
Diseases / complications. Medicare / statistics & numerical data. Myocardial Infarction / drug therapy. Thrombolytic Therapy / statistics & numerical data
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(PMID = 16183413.001).
[ISSN]
1523-6838
[Journal-full-title]
American journal of kidney diseases : the official journal of the National Kidney Foundation
[ISO-abbreviation]
Am. J. Kidney Dis.
[Language]
eng
[Grant]
United States / AHRQ HHS / HS / T32 HS013852; United States / NHLBI NIH HHS / HL / R01 HL70786
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Cardiovascular Agents; 0 / Fibrinolytic Agents; AYI8EX34EU / Creatinine
87.
Mazaris EM, Warrens AN, Papalois VE:
Ethical issues in live donor kidney transplant: views of medical and nursing staff.
Exp Clin Transplant
; 2009 Mar;7(1):1-7
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[Title]
Ethical issues in live donor
kidney
transplant: views of medical and nursing staff.
OBJECTIVES: The ongoing development of live donor
kidney
transplant has generated many ethical dilemmas.
MATERIALS AND METHODS: An anonymous and confidential questionnaire was sent to 236 members of the medical and nursing staff of the West London
Renal
and Transplant Centre, to assess their views on the ethics of the current practice of live donor
kidney
transplant.
Respondents considered live donor
kidney
transplant ethically acceptable between blood relatives (100%), nonblood relatives and friends (92.6%), and strangers (47.2%).
Most respondents were willing to donate a
kidney
to a blood relative (92.6%) or a nonblood relative or friend (81.5%), and 12.0% were willing to donate to a stranger.
Considering themselves as potential recipients if they had end-stage
renal
disease, most would accept a
kidney
from a blood relative (91.7%) or nonblood relative or friend (85.2%),while 44.5% would accept a
kidney
from a stranger.
CONCLUSIONS: Live related and unrelated
kidney
donation are considered ethically acceptable procedures, and nondirected donation is gaining support among transplant professionals.
[MeSH-major]
Attitude of Health Personnel. Directed Tissue Donation / ethics. Health Knowledge, Attitudes, Practice.
Kidney
Transplantation / ethics. Living Donors / ethics. Tissue and Organ Procurement / ethics
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(PMID = 19364304.001).
[ISSN]
1304-0855
[Journal-full-title]
Experimental and clinical transplantation : official journal of the Middle East Society for Organ Transplantation
[ISO-abbreviation]
Exp Clin Transplant
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Turkey
88.
Mozer P, Leroy A, Payan Y, Troccaz J, Chartier-Kastler E, Richard F:
Computer-assisted access to the kidney.
Int J Med Robot
; 2005 Dec;1(4):58-66
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[Title]
Computer-assisted access to
the kidney
.
OBJECTIVES: The aim of this paper is to introduce the principles of computer-assisted access to
the kidney
.
MATERIAL AND METHODS: Both CT and US images of informed normal volunteer were obtained to perform calculation on the accuracy of registration and punctures were carried out on a
kidney
phantom to measure the precision of the whole of the system.
RESULTS: We carried out millimetric registrations on real data and guidance experiments on a
kidney
phantom showed encouraging results of 4.7 mm between planned and reached targets.
[MeSH-major]
Kidney
/ surgery. Surgery, Computer-Assisted
HAL archives ouvertes.
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[Copyright]
Copyright 2005 John Wiley & Sons, Ltd.
(PMID = 17518406.001).
[ISSN]
1478-596X
[Journal-full-title]
The international journal of medical robotics + computer assisted surgery : MRCAS
[ISO-abbreviation]
Int J Med Robot
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
89.
Geel A, Zuidema W, van Gelder T, van Doornum G, Weimar W:
Successful vaccination against varicella zoster virus prior to kidney transplantation.
Transplant Proc
; 2005 Mar;37(2):952-3
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[Title]
Successful vaccination against varicella zoster virus prior to
kidney
transplantation.
BACKGROUND: In recent years we have observed a number of severe complications of primary varicella-zoster virus (VZV) infections after adult
kidney
transplantation.
We questioned how many patients on the waiting list for
kidney
transplantation had not been protected against VZV and whether patients with
renal
insufficiency would be able to develop a specific immune response upon VZV vaccination.
METHODS: We examined the VZV antibody titer of 280 patients on
the kidney
transplant waiting list.
Seronegative
kidney
transplant candidates were vaccinated twice with a live attenuated varicella vaccine at an interval of 6 weeks.
[MeSH-major]
Antibodies, Viral / blood. Chickenpox / immunology. Chickenpox Vaccine / therapeutic use.
Kidney
Transplantation / immunology
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(PMID = 15848586.001).
[ISSN]
0041-1345
[Journal-full-title]
Transplantation proceedings
[ISO-abbreviation]
Transplant. Proc.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Viral; 0 / Chickenpox Vaccine
90.
Bader AA, Tamussino KF, Winter R:
Ectopic (pelvic) kidney mimicking bulky lymph nodes at pelvic lymphadenectomy.
Gynecol Oncol
; 2005 Mar;96(3):873-5
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[Title]
Ectopic (pelvic)
kidney
mimicking bulky lymph nodes at pelvic lymphadenectomy.
BACKGROUND: Ectopic (pelvic)
kidney
is the most common congenital
renal
anomaly with an incidence of 1 in 500 to 1 in 2000.
A pelvic
kidney
can be encountered at pelvic or paraaortic lymphadenectomy.
CASE REPORTS: In two patients undergoing pelvic lymphadenectomy, lobulated
tumors
near the pelvic brim were initially interpreted as bulky lymph node conglomerates.
Further dissection showed the ureter to originate from the masses, leading to a
diagnosis of
pelvic
kidney
.
CONCLUSION: Pelvic
kidneys
mistaken for bulky lymph nodes are a potential intraoperative pitfall in patients with gynecologic malignancies.
Keys to recognition include an index of suspicion, identifying the course of the ureter and origin of the
renal
vessels, and confirming absence of a
kidney
at the normal location.
[MeSH-major]
Genital
Neoplasms
, Female / surgery.
Kidney
/ abnormalities. Lymph Nodes / surgery
[MeSH-minor]
Aged. Aged, 80 and over.
Diagnosis
, Differential. Female. Humans. Lymph Node Excision. Lymphatic Metastasis. Middle Aged
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(PMID = 15721442.001).
[ISSN]
0090-8258
[Journal-full-title]
Gynecologic oncology
[ISO-abbreviation]
Gynecol. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
91.
Mekeel KL, Mazur MJ, Reddy KS, Mulligan DC, Heilman RL, Chakkera HA, Andrews PE, Moss AA:
Diffuse parenchymal urine leak after kidney transplantation following degloving injury during donor nephrectomy.
Am J Transplant
; 2007 Aug;7(8):2039-41
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[Title]
Diffuse parenchymal urine leak after
kidney
transplantation following degloving injury during donor nephrectomy.
Laparoscopic donor nephrectomy can result in trauma to
the kidney
which may affect recipient graft function.
In this case,
the kidney
sustained a complete degloving of the capsule during extraction.
The kidney
was transplanted and had immediate, good
renal
function, but postoperative course was complicated by a large urinoma that drained through the wound.
Exploration was negative for a defined urine leak, but the surface of the denuded
kidney
was leaking a significant amount of unconcentrated urine.
The patient was successfully treated with tissue glue treatment to
the kidney
surface and peritoneal window.
[MeSH-major]
Intraoperative Complications.
Kidney
/ injuries.
Kidney
Transplantation / adverse effects. Laparoscopy / adverse effects. Nephrectomy / adverse effects. Tissue Donors. Tissue and Organ Procurement / methods
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(PMID = 17578504.001).
[ISSN]
1600-6135
[Journal-full-title]
American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
[ISO-abbreviation]
Am. J. Transplant.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Denmark
92.
Murugesan M, Courtauld E, Fisher C, Nathan S:
Renal capsular PEComa--a rare cause of surgically correctable renal hypertension.
Int Urol Nephrol
; 2007;39(3):705-7
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[Title]
Renal
capsular PEComa--a rare cause of surgically correctable
renal
hypertension.
This indicated a complex cystic lesion, measuring 2.4 x 5 x 10 cms , arising from the right
kidney
.
The mass was reported as a Perivascular Epitheloid Cell (PEC) lesion (PEComa) arising from the
renal
capsule.
Perivascular Epitheloid Cell
tumor
(PEComa), a recently defined
tumor
, is extremely rare.
PEComa's are usually
benign
, but cases have been reported in the literature which has an unfavourable outcome with metastatic dissemination.
We report this case because of its rarity and also
Renal
Capsular PEComa should be considered as a rare cause of
renal
hypertension, which can be surgically cured.
[MeSH-major]
Epithelioid Cells / pathology. Hypertension,
Renal
/ etiology.
Kidney Neoplasms
/ complications.
Neoplasms
, Connective Tissue / complications
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[Cites]
Histopathology. 2006 Jan;48(1):75-82
[
16359539.001
]
[Cites]
Pathology. 1991 Jul;23(3):185-8
[
1664078.001
]
[Cites]
Eur J Cancer. 1993;29A(13):1903-7
[
8260252.001
]
(PMID = 17318350.001).
[ISSN]
0301-1623
[Journal-full-title]
International urology and nephrology
[ISO-abbreviation]
Int Urol Nephrol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Netherlands
93.
Krajisnik T, Olauson H, Mirza MA, Hellman P, Akerström G, Westin G, Larsson TE, Björklund P:
Parathyroid Klotho and FGF-receptor 1 expression decline with renal function in hyperparathyroid patients with chronic kidney disease and kidney transplant recipients.
Kidney Int
; 2010 Nov;78(10):1024-32
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[Title]
Parathyroid Klotho and FGF-receptor 1 expression decline with
renal
function in hyperparathyroid patients with chronic
kidney
disease and
kidney
transplant recipients.
However, patients with chronic
kidney
disease (CKD) develop secondary hyperparathyroidism despite high levels of serum FGF23, indicating a parathyroid FGF23 'resistance'.
Here we analyzed the expression of the FGF23 receptors Klotho and FGF receptor 1 (FGFR1) in 88 hyperplastic parathyroid glands from 31 patients with CKD (including 21
renal
allograft recipients), and their regulation in isolated bovine and human hyperplastic parathyroid cells.
Thus parathyroid Klotho and FGFR1 decrease with declining
renal
function, possibly because of alterations in mineral metabolism related to the failing
kidney
.
[MeSH-major]
Glucuronidase / metabolism. Hyperparathyroidism / metabolism.
Kidney
/ physiopathology.
Kidney
Diseases / metabolism.
Kidney
Transplantation / physiology. Parathyroid Glands / metabolism. Receptors, Fibroblast Growth Factor / metabolism
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[CommentIn]
Kidney Int. 2010 Nov;78(10):953-5
[
21030971.001
]
(PMID = 20686451.001).
[ISSN]
1523-1755
[Journal-full-title]
Kidney international
[ISO-abbreviation]
Kidney Int.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Minerals; 0 / Parathyroid Hormone; 0 / Receptors, Calcitriol; 0 / Receptors, Fibroblast Growth Factor; 0 / fibroblast growth factor 23; 62031-54-3 / Fibroblast Growth Factors; EC 3.2.1.31 / Glucuronidase; EC 3.2.1.31 / klotho protein
94.
Bouman CS, Oudemans-van Straaten HM:
Timing of renal replacement therapy in critically ill patients with acute kidney injury.
Curr Opin Crit Care
; 2007 Dec;13(6):656-61
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[Title]
Timing of
renal
replacement therapy in critically ill patients with acute
kidney
injury.
PURPOSE OF REVIEW: Timing of
renal
replacement therapy in critically ill patients with acute
kidney
injury is highly subjective, and may influence outcome.
We discuss
renal
and nonrenal criteria for timing considering the recent literature.
All but one randomized controlled trial indicated better outcome with early
renal
replacement therapy but had poor methodological quality.
SUMMARY: In the absence of large randomized controlled trials we can make no firm recommendations for timing of
renal
replacement therapy in acute
kidney
injury.
Since rapid recovery of
renal
function is unlikely when other organ failure persists and the consequences of acute
kidney
injury may be more severe in critically ill patients, we suggest other organ failure is also considered.
Patients with acute
kidney
injury, persisting shock and poorly recovering functions of other organs may benefit from early therapy.
For future studies, we recommend describing
renal
replacement therapy timing according to the 'RIFLE' classification, as modified by the Acute
Kidney
Injury Network, and quantifying the severity of other organ failure.
Biomarkers may refine acute
kidney
injury and timing definitions in the future.
[MeSH-major]
Acute
Kidney
Injury / therapy. Critical Illness.
Kidney
/ injuries.
Renal
Replacement Therapy / methods. Treatment Outcome
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(PMID = 17975386.001).
[ISSN]
1070-5295
[Journal-full-title]
Current opinion in critical care
[ISO-abbreviation]
Curr Opin Crit Care
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers
[Number-of-references]
51
95.
Sudarshan S, Linehan WM:
Genetic basis of cancer of the kidney.
Semin Oncol
; 2006 Oct;33(5):544-51
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[Title]
Genetic basis of cancer of the
kidney
.
Kidney
cancer is not a single disease.
It is made up of a number of different types of cancer that occur in
the kidney
, each with a different histologic type, having a different clinical course, responding differently to therapy and caused by a different gene.
The identification of families with a predisposition to the development of
renal
neoplasms
, including von Hippel-Lindau (VHL), hereditary papillary
renal
carcinoma (HPRC), Birt-Hogg-Dubé (BHD), and hereditary leiomyomatosis and
renal
cell cancer (HLRCC), has made possible the identification of the different genes for these cancers.
The elucidation of molecular pathogenesis in these familial forms
of kidney
cancer should provide the opportunity to determine successful approaches for novel therapeutic agents.
[MeSH-major]
Carcinoma, Papillary / genetics. Carcinoma,
Renal
Cell / genetics. Genetic Predisposition to Disease.
Kidney Neoplasms
/ genetics. von Hippel-Lindau Disease / genetics
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(PMID = 17045083.001).
[ISSN]
0093-7754
[Journal-full-title]
Seminars in oncology
[ISO-abbreviation]
Semin. Oncol.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural; Review
[Publication-country]
United States
[Number-of-references]
87
96.
Kalb B, Martin DR, Salman K, Sharma P, Votaw J, Larsen C:
Kidney transplantation: structural and functional evaluation using MR Nephro-Urography.
J Magn Reson Imaging
; 2008 Oct;28(4):805-22
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[Title]
Kidney
transplantation: structural and functional evaluation using MR Nephro-Urography.
End-stage-
renal
disease (ESRD) is a major health issue in the United States, and the Medicare costs of ESRD totaled nearly USD 21 billion in 2005.
Renal
transplantation has emerged as the treatment of choice in this patient population, providing improved quality of life and lower healthcare costs compared with other treatment options.
Imaging evaluation of a graft
kidney
plays a critical role in the postoperative care of the
renal
transplant patient.
In the past, diagnostic evaluation of the transplant
kidney
has depended upon a combination of ultrasonography, computed tomography, MRI, and biopsy, used in conjunction with the patient's clinical presentation.
However, new and developing advances in MR technology has lead to the development of MR Nephro-Urography (MRNU), which provides both anatomic and functional evaluation of the
kidney
in a single examination.
It is expected that the increasing use of MRNU will have a significant impact on the management of
renal
transplant patients.
This review describes MRNU methodology, examines known posttransplant complications, and highlights the utility of MRNU as a comprehensive imaging examination to diagnose both surgical and medical complications of the transplant
kidney
.
[MeSH-major]
Kidney
/ blood supply.
Kidney
Failure, Chronic / surgery.
Kidney
Transplantation. Magnetic Resonance Imaging / methods. Postoperative Complications /
diagnosis
[MeSH-minor]
Graft Rejection. Graft Survival. Humans. Recovery of Function.
Renal
Dialysis
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[Copyright]
(c) 2008 Wiley-Liss, Inc.
(PMID = 18821623.001).
[ISSN]
1053-1807
[Journal-full-title]
Journal of magnetic resonance imaging : JMRI
[ISO-abbreviation]
J Magn Reson Imaging
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
64
97.
Olson GE, Winfrey VP, Hill KE, Burk RF:
Megalin mediates selenoprotein P uptake by kidney proximal tubule epithelial cells.
J Biol Chem
; 2008 Mar 14;283(11):6854-60
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[Title]
Megalin mediates selenoprotein P uptake by
kidney
proximal tubule epithelial cells.
Selenoprotein P (Sepp1) contains most of the selenium in blood plasma, and it is utilized by
the kidney
, brain, and testis as a selenium source for selenoprotein synthesis.
We recently demonstrated that apolipoprotein E receptor-2 (ApoER2) is required for Sepp1 uptake by the testis and that deletion of ApoER2 reduces testis and brain, but not
kidney
, selenium levels.
This study examined
the kidney
Sepp1 uptake pathway.
Tissue ligand binding assays using cryosections of Sepp1-/-
kidneys
revealed that the proximal tubule epithelium contained Sepp1-binding sites that were blocked by the receptor-associated protein, RAP, an inhibitor of lipoprotein receptor-ligand interactions.
Ligand blotting assays
of kidney
membrane preparations fractionated by SDS-PAGE revealed that Sepp1 binds megalin, a lipoprotein receptor localized to the proximal tubule epithelium.
Immunolocalization analyses confirmed the in vivo co-localization of Sepp1 and megalin in wild type
kidneys
and demonstrated the absence of proximal tubule Sepp1 uptake in megalin null mice.
These results demonstrate that
kidney
selenium homeostasis is mediated by a megalin-dependent Sepp1 uptake pathway in the proximal tubule.
[MeSH-major]
Epithelial Cells / metabolism. Gene Expression Regulation.
Kidney
Tubules / cytology. Low Density Lipoprotein Receptor-Related Protein-2 / physiology. Selenoprotein P / metabolism
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(PMID = 18174160.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Grant]
United States / NIEHS NIH HHS / ES / ES02497; United States / NICHD NIH HHS / HD / HD044863
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / LDL-Receptor Related Proteins; 0 / Low Density Lipoprotein Receptor-Related Protein-2; 0 / Receptors, Lipoprotein; 0 / Selenoprotein P; 0 / low density lipoprotein receptor-related protein 8
98.
Mabrut JY, Boulez J, Peix JL, Gigot JF, Gouillat C, de La Roche E, Ducerf C, Baulieux J:
Laparoscopic pancreatic resection: a preliminary experience of 15 patients.
Hepatogastroenterology
; 2005 Jan-Feb;52(61):230-2
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METHODOLOGY: 15 consecutive patients suffering from
benign
cystic pancreatic (n=6), neuroendocrine
tumors
(n=8) or pancreatic metastasis from
renal
carcinoma (n=1) undergoing laparoscopic pancreatic resection were retrospectively collected from 5 academic hospitals.
RESULTS: Laparoscopic procedure was completed in 10 patients, including 7 distal pancreatectomies (with 5 spleen preservation), 2
tumor
enucleations and 1 partial cystic resection.
CONCLUSIONS: Laparoscopic pancreatic resection is feasible for distal pancreatic
tumors
.
[MeSH-major]
Cystadenoma / surgery. Laparoscopy. Neuroendocrine
Tumors
/ surgery. Pancreatectomy. Pancreatic
Neoplasms
/ surgery
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Female. Humans.
Kidney Neoplasms
/ pathology. Male. Middle Aged. Retrospective Studies. Treatment Outcome
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(PMID = 15783037.001).
[ISSN]
0172-6390
[Journal-full-title]
Hepato-gastroenterology
[ISO-abbreviation]
Hepatogastroenterology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
99.
Patel TY, Hovsepian DM, Duncan JR:
Measurement of blood flow before and after embolization with use of fluorescent microspheres in an animal model.
J Vasc Interv Radiol
; 2006 Jan;17(1):103-11
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PURPOSE: Catheter-directed embolization has become a widespread technique for the treatment of
benign
and malignant
neoplasms
.
The mechanism whereby embolization leads to selective atrophy of these
neoplasms
is largely speculative.
As a potential model for the large regional perfusion differences between normal and neoplastic tissues,
renal
perfusion was studied before and after catheter-directed embolization.
The working hypothesis was that embolization would create measurable changes in blood flow in the
renal
cortex and medulla.
MATERIALS AND METHODS: Microspheres (l0 microm in diameter) containing a series of different fluorophores were injected into the arterial system before and after the
renal
arteries were embolized with a series of larger (100-300 microm) particulate embolic agents.
The distribution of the microspheres in the
renal
cortex,
renal
medulla, and liver was analyzed by fluorescence microscopy as well as by extraction of the fluorophores.
Before embolization, the
renal
cortex received approximately three times more flow than the medulla.
After embolization, perfusion of the
renal
cortex and medulla decreased in parallel.
The fact that parallel decreases in flow were found in the
renal
cortex and medulla indicates that the distribution of each embolic agent was flow-directed.
These results might provide insight into the mechanism of
tumor
atrophy after uterine artery embolization or hepatic chemoembolization.
[MeSH-major]
Embolization, Therapeutic.
Kidney Neoplasms
/ therapy. Microspheres.
Renal
Circulation
[MeSH-minor]
Animals. Female. Fluorescent Dyes / administration & dosage.
Kidney
Cortex / blood supply.
Kidney
Medulla / blood supply. Microscopy, Fluorescence. Models, Animal. Rabbits. Radiography, Interventional.
Renal
Artery
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